Статті в журналах: "F11A"

1

Ottaviano, Emerenziana, Elisa Borghi, Laura Giovati, Monica Falleni, Delfina Tosi, Walter Magliani, Giulia Morace, Stefania Conti, and Tecla Ciociola. "Therapeutic Effect of an Antibody-Derived Peptide in a Galleria mellonella Model of Systemic Candidiasis." International Journal of Molecular Sciences 22, no. 20 (October 9, 2021): 10904. http://dx.doi.org/10.3390/ijms222010904.

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The synthetic peptide T11F (TCRVDHRGLTF), with sequence identical to a fragment of the constant region of human IgM, and most of its alanine-substituted derivatives proved to possess a significant candidacidal activity in vitro. In this study, the therapeutic efficacy of T11F, D5A, the derivative most active in vitro, and F11A, characterized by a different conformation, was investigated in Galleria mellonella larvae infected with Candida albicans. A single injection of F11A and D5A derivatives, in contrast with T11F, led to a significant increase in survival of larvae injected with a lethal inoculum of C. albicans cells, in comparison with infected animals treated with saline. Peptide modulation of host immunity upon C. albicans infection was determined by hemocyte analysis and larval histology, highlighting a different immune stimulation by the studied peptides. F11A, particularly, was the most active in eliciting nodule formation, melanization and fat body activation, leading to a better control of yeast infection. Overall, the obtained data suggest a double role for F11A, able to simultaneously target the fungus and the host immune system, resulting in a more efficient pathogen clearance.

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2

Massie, Steven T., A. Goldman, David G. Murcray, and John C. Gille. "Approximate absorption cross sections of F12, F11, C1ONO_2, N_2O_5, HNO_3, CCl_4, CF_4, F21, F113, F114, and HNO_4." Applied Optics 24, no. 21 (November 1, 1985): 3426. http://dx.doi.org/10.1364/ao.24.003426.

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3

Pertinhez, Thelma A., Tecla Ciociola, Laura Giovati, Walter Magliani, Silvana Belletti, Luciano Polonelli, Stefania Conti, and Alberto Spisni. "Dissection of the Structural Features of a Fungicidal Antibody-Derived Peptide." International Journal of Molecular Sciences 19, no. 12 (November 28, 2018): 3792. http://dx.doi.org/10.3390/ijms19123792.

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The synthetic peptide T11F (TCRVDHRGLTF), derived from the constant region of human IgM antibodies, proved to exert a significant activity in vitro against yeast strains, including multidrug resistant isolates. Alanine substitution of positively charged residues led to a decrease in candidacidal activity. A more dramatic reduction in activity resulted from cysteine replacement. Here, we investigated the conformational properties of T11F and its alanine-substituted derivatives by circular dichroism (CD) and nuclear magnetic resonance (NMR) spectroscopy. Peptide interaction with Candida albicans cells was studied by confocal and scanning electron microscopy. T11F and most of its derivatives exhibited CD spectra with a negative band around 200 nm and a weaker positive band around 218 nm suggesting, together with NMR coupling constants, the presence of a polyproline II (PPII) helix, a conformational motif involved in a number of biological functions. Analysis of CD spectra revealed a critical role for phenylalanine in preserving the PPII helix. In fact, only the F11A derivative presented a random coil conformation. Interestingly, the loss of secondary structure influenced the rate of killing, which turned out to be significantly reduced. Overall, the obtained results suggest that the PPII conformation contributes in characterising the cell penetrating and fungicidal properties of the investigated peptides.

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4

Kobayashi, Hiyori, Teizo Asano, Tomohiro Tanaka, Hiroyuki Suzuki, Mika K. Kaneko, and Yukinari Kato. "Determination of the Binding Epitope of an Anti-Mouse CCR9 Monoclonal Antibody (C9Mab-24) Using the 1× Alanine and 2× Alanine-Substitution Method." Antibodies 12, no. 1 (January 31, 2023): 11. http://dx.doi.org/10.3390/antib12010011.

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C-C chemokine receptor 9 (CCR9) is a receptor for C-C-chemokine ligand 25 (CCL25). CCR9 is crucial in the chemotaxis of immune cells and inflammatory responses. Moreover, CCR9 is highly expressed in tumors, including several solid tumors and T-cell acute lymphoblastic leukemia. Several preclinical studies have shown that anti-CCR9 monoclonal antibodies (mAbs) exert antitumor activity. Therefore, CCR9 is an attractive target for tumor therapy. In this study, we conducted the epitope mapping of an anti-mouse CCR9 (mCCR9) mAb, C9Mab-24 (rat IgG2a, kappa), using the 1× alanine (1× Ala)- and 2× alanine (2× Ala)-substitution methods via enzyme-linked immunosorbent assay. We first performed the 1× Ala-substitution method using one alanine-substituted peptides of the mCCR9 N-terminus (amino acids 1–19). C9Mab-24 did not recognize two peptides (F14A and F17A), indicating that Phe14 and Phe17 are critical for C9Mab-24-binding to mCCR9. Furthermore, we conducted the 2× Ala-substitution method using two consecutive alanine-substituted peptides of the mCCR9 N-terminus, and showed that C9Mab-24 did not react with four peptides (M13A–F14A, F14A–D15A, D16A–F17A, and F17A–S18A), indicating that 13-MFDDFS-18 is involved in C9Mab-24-binding to mCCR9. Overall, combining, the 1× Ala- or 2× Ala-scanning methods could be useful for understanding for target–antibody interaction.

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5

Babinska, Anna, Bani Azari, Moro Salifu, Ruijie Liu, Xian-Cheng Jiang, Malgorzata Sobocka, Dorothy Boo, et al. "The F11 receptor (F11R/JAM-A) in atherothrombosis: Overexpression of F11R in atherosclerotic plaques." Thrombosis and Haemostasis 97, no. 02 (2007): 272–81. http://dx.doi.org/10.1160/th06-08-0454.

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SummaryF11R is the gene name for an adhesion protein, called the F11-receptor, aka JAM-A, which under normal physiological conditions is expressed constitutively on the surface of platelets and localized within tight junctions of endothelial cells (EC). Previous studies of the interactions between human platelets and EC suggested that F11R/JAM-A plays a crucial role in inflammatory thrombosis and atherosclerosis. The study reported here obtained in-vivo confirmation of this conclusion by investigating F11R/JAM-A protein and mRNA in patients with aortic and peripheral vascular disease and in an animal model of atherosclerosis. Molecular and immunofluorescence determinations revealed very high levels of F11R/JAM-A mRNA and F11R/JAM-A protein in atherosclerotic plaques of cardiovascular patients. Similar results were obtained with 12-week-old atherosclerosis-prone apoE-/- mice, an age in which atherosclerotic plaques are well established. Enhanced expression of the F11R/JAM-A message in cultured EC from human aortic and venous vessels was observed following exposure of the cells to cytokines. Determinations of platelet adhesion to cultured EC inflamed by combined cytokine treatment in the presence of F11R/JAM-A – antagonists provided data indicating that de novo expression of F11R/JAM-A on the luminal surface of inflamed EC has an important role in the conversion of EC to a thrombogenic surface. Further studies of these interactions under flow conditions and under in-vivo settings could provide a final proof of a causal role for F11R/JAM-A in the initiation of thrombosis. Based on our invitro and in-vivo studies to date, we propose that therapeutic drugs which antagonize the function of F11R/JAM-A should be tested as novel means for the prevention and treatment of atherosclerosis, heart attacks and stroke.

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6

Babinska, Anna, Tahir Ahmed, Olcay Batuman, Yigal Ehrlich, M. Hussain, Mamdouh Kedees, Humra Athar, and Elizabeth Kornecki. "F11-Receptor (F11R/JAM) Mediates Platelet Adhesion to Endothelial Cells: Role in Inflammatory Thrombosis." Thrombosis and Haemostasis 88, no. 11 (2002): 843–50. http://dx.doi.org/10.1055/s-0037-1613312.

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SummaryThe F11 receptor (F11R) is a cell adhesion molecule (CAM), member of the immunoglobulin superfamily found on the surface of human platelets, and determined to play a role in platelet aggregation, secretion, adhesion and spreading. The same molecule is present also at tight junctions of endothelial cells (EC) where it is known as JAM and acts as a CAM through homophilic interactions. The role of F11R/JAM in the interaction of platelets with endothelial cells was investigated in the current studies. We report here that washed human platelets adhere specifically to a matrix made of immobilized, recombinant sF11R. Furthermore, platelets adhere to cytokine(TNF-α, INF-γ) stimulated human umbilical vein endothelial cells (HUVEC), and approximately 40-60% of the adhesive force is exerted by homophilic interactions between the F11R of platelets and EC. This is evidenced by the inhibition of platelet adhesion to endothelial cells by recombinant soluble form of the F11R, and by two F11R peptides with amino acid sequences of the N-terminal region, and in the 1st Ig fold of the F11R, respectively. This study suggests a role for F11R in the adhesion of platelets to cytokine-inflamed endothelial cells and thus in thrombosis and atherosclerosis induced in non-denuded blood vessels by inflammatory processes. Agents that block the F11R-mediated adhesion of platelets to EC may be of therapeutic value in controlling thrombosis and preventing heart attacks and stroke.

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7

Sobocka, Malgorzata B., Tomasz Sobocki, Probal Banerjee, Cipora Weiss, Julie I. Rushbrook, Allen J. Norin, John Hartwig, et al. "Cloning of the human platelet F11 receptor: a cell adhesion molecule member of the immunoglobulin superfamily involved in platelet aggregation." Blood 95, no. 8 (April 15, 2000): 2600–2609. http://dx.doi.org/10.1182/blood.v95.8.2600.

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Abstract This study demonstrates that the human platelet F11 receptor (F11R) functions as an adhesion molecule, and this finding is confirmed by the structure of the protein as revealed by molecular cloning. The F11R is a 32-/35-kd protein duplex that serves as the binding site through which a stimulatory monoclonal antibody causes platelet aggregation and granule secretion. A physiological role for the F11R protein was demonstrated by its phosphorylation after the stimulation of platelets by thrombin and collagen. A pathophysiological role for the F11R was revealed by demonstrating the presence of F11R-antibodies in patients with thrombocytopenia. Adhesion of platelets through the F11R resulted in events characteristic of the action of cell adhesion molecules (CAMs). To determine the structure of this protein, we cloned the F11R cDNA from human platelets. The predicted amino acid sequence demonstrated that it is an integral membrane protein and an immunoglobulin superfamily member containing 2 extracellular C2-type domains. The structure of the F11R as a member of a CAM family of proteins and its activity in mediating adhesion confirm each another. We conclude that the F11R is a platelet-membrane protein involved in 2 distinct processes initiated on the platelet surface. The first is antibody-induced platelet aggregation and secretion that are dependent on both the FcγRII and the GPIIb/IIIa integrin and that may be involved in pathophysiological processes associated with certain thrombocytopenias. The second is an F11R-mediated platelet adhesion that is not dependent on either the FcγRII or the fibrinogen receptor and that appears to play a role in physiological processes associated with platelet adhesion and aggregation.

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8

Sobocka, Malgorzata B., Tomasz Sobocki, Probal Banerjee, Cipora Weiss, Julie I. Rushbrook, Allen J. Norin, John Hartwig, et al. "Cloning of the human platelet F11 receptor: a cell adhesion molecule member of the immunoglobulin superfamily involved in platelet aggregation." Blood 95, no. 8 (April 15, 2000): 2600–2609. http://dx.doi.org/10.1182/blood.v95.8.2600.008k28_2600_2609.

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This study demonstrates that the human platelet F11 receptor (F11R) functions as an adhesion molecule, and this finding is confirmed by the structure of the protein as revealed by molecular cloning. The F11R is a 32-/35-kd protein duplex that serves as the binding site through which a stimulatory monoclonal antibody causes platelet aggregation and granule secretion. A physiological role for the F11R protein was demonstrated by its phosphorylation after the stimulation of platelets by thrombin and collagen. A pathophysiological role for the F11R was revealed by demonstrating the presence of F11R-antibodies in patients with thrombocytopenia. Adhesion of platelets through the F11R resulted in events characteristic of the action of cell adhesion molecules (CAMs). To determine the structure of this protein, we cloned the F11R cDNA from human platelets. The predicted amino acid sequence demonstrated that it is an integral membrane protein and an immunoglobulin superfamily member containing 2 extracellular C2-type domains. The structure of the F11R as a member of a CAM family of proteins and its activity in mediating adhesion confirm each another. We conclude that the F11R is a platelet-membrane protein involved in 2 distinct processes initiated on the platelet surface. The first is antibody-induced platelet aggregation and secretion that are dependent on both the FcγRII and the GPIIb/IIIa integrin and that may be involved in pathophysiological processes associated with certain thrombocytopenias. The second is an F11R-mediated platelet adhesion that is not dependent on either the FcγRII or the fibrinogen receptor and that appears to play a role in physiological processes associated with platelet adhesion and aggregation.

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9

Babinska, Anna, Mamdouh Kedees, Humra Athar, Tomasz Sobocki, Malgorzata Sobocka, Tahir Ahmed, Yigal Ehrlich, M. Hussain, and Elizabeth Kornecki. "Two Regions of the Human Platelet F11-Receptor (F11R) Are Critical for Platelet Aggregation, Potentiation and Adhesion." Thrombosis and Haemostasis 87, no. 04 (2002): 712–21. http://dx.doi.org/10.1055/s-0037-1613070.

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SummaryThe F11 receptor (F11R) was first identified on the surface of human platelets as a target for a stimulatory monoclonal antibody (M.Ab.F11) that induces secretion, followed by exposure of fibrinogen receptors and aggregation. Cloning of the gene of F11R has revealed that this protein is a cell adhesion molecule (CAM), a member of the Ig superfamily and an ortholog of the murine protein called junctional adhesion molecule (JAM). The present study has identified two domains through which M.Ab.F11 triggers a platelet response culminating with aggregation. M.Ab.F11-mediated platelet adhesion, and the potentiation of collagen and ADP-induced platelet aggregation by M.Ab.F11, were found to involve the same two domains. A F11R recombinant protein (sF11R) completely inhibited platelet aggregation, adhesion and potentiation induced by M.Ab.F11, indicative that the active conformation of the external domain of F11R is present in the soluble, secreted recombinant protein. Furthermore, a specific peptide containing the sequence of the N-terminal amino acids S-1 to C-23 of F11R, and a peptide with the sequence of K-70 to C-82 in the 1st immunoglobulin-like (Ig) fold of F11R, both inhibited M.Ab.F11-induced aggregation, adhesion and potentiation of the aggregation of human platelets. Modeling of the 3D structure of the extracellular domain of the human platelet F11R suggests that these two regions form an active site within the conformation of this CAM. The sequence of these functional domains of F11R (in the N-terminus and 1st Ig-fold) provide the basis for new drug development in the treatment of certain types of thrombocytopenia and inflammatory thrombosis.

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10

Chagas, Edvan Alves, Jairo Osvaldo Cazetta, Eliana Gertrudes Macedo Lemos, Moacir Pasqual, Antonio de Goes, Jose Darlan Ramos, Rafael Pio, Wilson Barbosa, Vander Mendonça, and Luis Alberto Ambrosio. "Identificação de híbridos de citros resistentes à mancha-marrom-de-alternária por meio de fAFLP e testes de patogenicidade." Pesquisa Agropecuária Brasileira 42, no. 7 (July 2007): 975–83. http://dx.doi.org/10.1590/s0100-204x2007000700009.

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O objetivo deste trabalho foi identificar híbridos, oriundos de hibridações controladas entre 'Folha Murcha' x 'Ponkan' e testá-los quanto à resistência a Alternaria alternata f. sp. citri. As plântulas foram obtidas via cultura in vitro de embriões. Utilizou-se o marcador molecular fAFLP para identificação dos híbridos e, em seguida, realizou-se o teste de patogenicidade nos híbridos com isolados de Alternaria alternata f. sp. citri, em condições de laboratório. Os pares de primers EcoRI AAG - MseI CAG e EcoRI ACC - MseI CAA foram os mais eficientes na identificação dos híbridos, os quais identificaram 48,5% de híbridos. Os híbridos F64, F108, F111, F113, F131 e F139 são potencialmente resistentes a Alternaria alternata f. sp. citri.

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11

Babinska, A., C. C. Clement, M. Swiatkowska, J. Szymanski, A. Shon, Y. H. Ehrlich, E. Kornecki, and M. O. Salifu. "Development of new antiatherosclerotic and antithrombotic drugs utilizing F11 receptor (F11R/JAM-A) peptides." Biopolymers 102, no. 4 (July 2014): 322–34. http://dx.doi.org/10.1002/bip.22503.

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12

Azari, Bani M., Danielle F. Joseph, Marc J. Braunstein, H. Uwe Klueppelberg, Eric LP Smith, Sadeaqua Scott, Jonathan D. Marmur, Anna Babinska, and Olcay Batuman. "Junctional Adhesion Molecule-A/F11 Receptor (JAM-A/F11R) Is a Novel Biomarker and a Potential Treatment Target In Multiple Myeloma Tumor and Its Microvascular Milieu." Blood 116, no. 21 (November 19, 2010): 450. http://dx.doi.org/10.1182/blood.v116.21.450.450.

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Abstract Abstract 450 Background: Multiple myeloma (MM) is a disease of clonal plasma cells that accumulate in the bone marrow (BM), causing monoclonal immunoglobulin (IG) production, BM failure, osteolytic lesions, and kidney disease. Although initially treatable, tumor cells ultimately become resistant to drug-treatment, and the disease is invariably fatal. Therefore, novel treatment targets need to be identified. The tumor microenvironment, and vascular endothelial cells in particular, play a key role in the adhesion and migration of MM cells and thus govern tumor survival and growth, as well as the acquisition of drug-resistance. Hence, the adhesion/migration systems of MM cells are key potential therapeutic targets. The cell membrane protein JAM-A/F11R is an endothelial cell (EC) adhesion molecule of the IG superfamily, and its expression is upregulated by TNF-a through NF-κB signaling. F11R also alters EC migration and paracellular permeability via stabilization of β1 integrin. We have previously shown that F11R gene expression and serum levels are upregulated in patients with MM compared to healthy controls. In this study, we further explored the functions of F11R within MM cells in order to gain insight into the potential role of this molecule in the progression and treatment of MM. Methods: The MM cell line RPMI-8266 (RPMI) was examined for functional studies in vitro. Informed consent was obtained from all subjects. Primary BM tumor cells were enriched to > 95% CD138+ cells by positive selection using anti-CD138 MACS MicroBeads. The CD138– fraction was used for outgrowth of confluent EPCs (> 98% vWF/CD133/KDR+). Human umbilical vein endothelial cells (HUVECs) served as controls. F11R mRNA levels were assessed by Affymetrix GeneChip analysis and by F11R probe-based real-time PCR compared to a standard curve normalized to GAPDH mRNA levels. F11R protein levels were measured by immunofluorescence (IF) and flow cytometry. The role of F11R in MM cell migration and survival was quantified by examining these functions in RPMI cells in which F11R was knocked down by siRNA silencing and comparing them with control untransfected RPMI cells or cells transfected with a non-targeting siRNA or lipofectamine. Tumor migration and survival were determined by the Millipore QCM Chemotaxis assay (using a 5 micron pore size) and an Promega Cell Proliferation Assay, respectively. Each assay was performed in triplicate and replicated at least twice. Statistical analyses were performed using Student's t-test, two-tailed; P≤.05 was considered significant. Results: Inhibition of F11R gene expression by siRNA resulted in 70% cell death compared to control untransfected (P<.001), non-targeting siRNA (P=.04), or lipofectamine-treated (P=.003) MM cells (RPMI). Moreover, migration of MM cells was also inhibited by 23% after silencing of F11R expression compared to cells transfected with control siRNA (P=.008). Elevated F11R mRNA levels in MM cell lines and patient-derived tumor endothelial progenitor cells (EPCs) was confirmed by IF and flow cytometry using a specific monoclonal antibody, and showed increased expression of both membrane and cytoplasmic F11R compared to controls. Gene expression profiles from 20 patients' corresponding BM tumor cells and EPCs showed that F11R mRNA levels in tumor cells were higher than MM in EPCs by 12.62 fold, (P=1×10-4). However, F11R had a higher level of expression in MM EPCs compared to healthy control EPCs by 2.41 fold (P=.001), reflecting a complex regulatory role of F11 signaling in MM, similar to breast cancer cells (Naik et al., 2008). Conclusion: We show, for the first time, that targeted inhibition of F11R/JAM-A expression bears key anti-myeloma consequences, defined by inhibition of tumor migration and survival. Taken together with elevated gene and protein expression of F11R/JAM-A expression, these results underscore the importance of this receptor as a tumor biomarker and a potential MM treatment target that warrants further validation. Future studies: Under investigation are the in vivo effect of F11R silencing in combination with other anti-myeloma strategies in a murine myeloma model; and also, whether F11R effects on MM cell migration involve stabilization of β1 integrin, as recently described in cardiovascular disease by Azari BM et al. 2010. Disclosures: No relevant conflicts of interest to declare.

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13

Bednarek, Radoslaw, Anna Selmi, Dagmara Wojkowska, Kamil Karolczak, Marcin Popielarski, Marta Stasiak, Moro O. Salifu, Anna Babinska, and Maria Swiatkowska. "Functional inhibition of F11 receptor (F11R/junctional adhesion molecule-A/JAM-A) activity by a F11R-derived peptide in breast cancer and its microenvironment." Breast Cancer Research and Treatment 179, no. 2 (October 24, 2019): 325–35. http://dx.doi.org/10.1007/s10549-019-05471-x.

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Abstract Purpose To examine the involvement of the F11R/JAM-A protein in breast cancer metastasis, we utilized the F11R/JAM-A antagonistic peptide 4D (P4D) in experiments of transendothelial migration (TEM) of breast cancer cells. Methods Experiments were conducted in the mouse 4T1 breast cancer model utilizing the human mammary epithelial cell and endothelial cell lines. The levels of soluble F11R/JAM-A (sJAM-A) in the murine plasmas were measured by ELISA. Levels of F11R/JAM-A mRNA and protein in cell lines were assessed by qRT-PCR and Western blot, respectively. Cell surface expression of F11R/JAM-A was demonstrated by flow cytometry. Functional tests included the TEM of breast cancer cells and adhesion of breast cancer cells to the endothelium. The endothelial permeability was studied by fluorescent tracer assay and by the Real-Time Cell Analysis (RTCA). Results The tumor inducers Tβ4 and TGF-β1 reduced the levels of sJAM-A in murine plasma, and reduced the F11R/JAM-A protein levels in the human microvascular endothelial cell line HMEC-1. The adhesion and TEM measured between breast cancer cells and inflamed or Tβ4-treated endothelium were inhibited by P4D. The presence of P4D did not destabilize the pre-existing tight junctions in the endothelial monolayer. The barrier-protecting effect of P4D was stronger than that of forskolin, when a booster dose of P4D was applied to the inflamed endothelium. Conclusions F11R/JAM-A protein can be considered as a novel target in the treatment of breast cancer metastasis. In vivo and clinical studies are needed to further investigate the effectiveness of F11R/JAM-A-derived peptide as a possible anti-metastatic drug.

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14

Sobocka, Malgorzata B., Tomasz Sobocki, Anna Babinska, John H. Hartwig, Mengru Li, Yigal H. Ehrlich, and Elizabeth Kornecki. "Signaling Pathways of the F11 Receptor (F11R; a.k.a. JAM-1, JAM-A) in Human Platelets: F11R Dimerization, Phosphorylation and Complex Formation with the Integrin GPIIIa." Journal of Receptors and Signal Transduction 24, no. 1-2 (January 2004): 85–105. http://dx.doi.org/10.1081/rrs-120034252.

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15

Ong, K. L., R. Y. H. Leung, A. Babinska, M. O. Salifu, Y. H. Ehrlich, E. Kornecki, L. Y. F. Wong, et al. "Elevated Plasma Level of Soluble F11 Receptor/Junctional Adhesion Molecule-A (F11R/JAM-A) in Hypertension." American Journal of Hypertension 22, no. 5 (May 1, 2009): 500–505. http://dx.doi.org/10.1038/ajh.2009.23.

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16

Kedees, Mamdouh H., Anna Babinska, M. Mahmood Hussain, Elizabeth Kornecki, Jonathan Deitch, Yigal H. Ehrlich, and Maria Swiatkowska. "Expression of a recombinant protein of the platelet F11 receptor (F11R) (JAM-1/JAM-A) in insect cells: F11R is naturally phosphorylated in the extracellular domain." Platelets 16, no. 2 (March 2005): 99–109. http://dx.doi.org/10.1080/09537100400010329.

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17

Kedees, Mamdouh H., Anna Babinska, Maria Swiatkowska, Jonathan Deitch, M. Mahmood Hussain, Yigal H. Ehrlich, and Elizabeth Kornecki. "Expression of a recombinant protein of the platelet F11 receptor (F11R) (JAM-1/JAM-A) in insect cells: F11R is naturally phosphorylated in the extracellular domain." Platelets 16, no. 3-4 (January 2005): 249. http://dx.doi.org/10.1080/09537100500186466.

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18

Cavusoglu, Erdal, Elizabeth Kornecki, Malgorzata B. Sobocka, Anna Babinska, Yigal H. Ehrlich, Vineet Chopra, Sunitha Yanamadala, et al. "Association of Plasma Levels of F11 Receptor/Junctional Adhesion Molecule-A (F11R/JAM-A) With Human Atherosclerosis." Journal of the American College of Cardiology 50, no. 18 (October 2007): 1768–76. http://dx.doi.org/10.1016/j.jacc.2007.05.051.

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19

Sobocki, T., M. B. Sobocka, A. Babinska, Y. H. Ehrlich, P. Banerjee, and E. Kornecki. "Genomic structure, organization and promoter analysis of the human F11R/F11 receptor/junctional adhesion molecule-1/JAM-A." Gene 366, no. 1 (January 2006): 128–44. http://dx.doi.org/10.1016/j.gene.2005.08.025.

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20

Zhang, HaiDi, RenDan Zhang, Jiaxin Yao, XianHua Hu, Yu Pu, Shuai He, Jinchuan Yu, Huiling Zhu, Bo Mu, and ChunYan Zhao. "Effect of F11R Gene Knockdown on Malignant Biological Behaviors of Pancreatic Cancer Cells." Journal of Oncology 2022 (March 7, 2022): 1–8. http://dx.doi.org/10.1155/2022/3379027.

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F11R receptor (F11R/junctional adhesion molecule-A/F11R-A) is preferentially concentrated at tight junctions and influences epithelial cell morphology and migration. Numerous studies have shown that the aberrant expression of F11R contributes to tumor progression including pancreatic cancer. However, the significance of F11R in various tumors is controversial, and the role of F11R in regulating the malignant behaviors of human pancreatic cancer is unknown. To investigate the role of F11R in the carcinogenesis of pancreatic cancer and the potential targets of F11R as a therapeutic target for pancreatic cancer, we knocked down F11R in the pancreatic cancer cell line PANC-1 using lentiviral approaches. We found that F11R silencing led to decreased cell proliferation, a loss of cell invasiveness, cell cycle arrest in the G1 phase, and enhanced cell apoptosis. The present results suggest that F11R may be a promising therapeutic target for pancreatic cancer.

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21

Azari, Bani M., Marc J. Braunstein, H. Uwe Kluppelberg, Sadeaqua S. Scott, Eric LP Smith, Jonathan D. Marmur, Anna Babinska, and Olcay Batuman. "Junctional Adhesion Molecule-A/ F11 Receptor (JAM-A/ F11R) Expression in Multiple Myeloma (MM): a Candidate Biomarker of Aggressive Disease." Blood 114, no. 22 (November 20, 2009): 2830. http://dx.doi.org/10.1182/blood.v114.22.2830.2830.

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Abstract Abstract 2830 Poster Board II-806 Background: Multiple myeloma (MM) is an incurable disease of clonal plasma cells that accumulate in the bone marrow (BM), causing monoclonal IG production, bone marrow failure, osteolytic lesions and kidney disease. Although initially treatable, MM ultimately becomes refractory to treatment, and is invariably fatal, when tumor cells that harbor genetic mutations expand without regulation. Therefore novel treatment targets need to be identified. A key mechanism in MM pathogenesis is regulation of tumor growth by the bone marrow (BM) microenvironment, particularly by bone marrow neo-vascularization and adhesion of tumor cells to the marrow stroma. Aberrantly expressed genes that regulate angiogenesis by MM cells enhance MM progression and constitute targets in its treatment. JAM-A/F11R is an endothelial cell (EC) adhesion molecule of the immunoglobulin superfamily which is a multifunctional cell membrane protein that mediates intracellular signaling events that alter EC migration and paracellular permeability. For example, in breast cancer, attenuation of JAM-A increases tumor invasion and metastasis through a decrease in tumor adhesion (Ulas Naik Cell Adh Migr. 2008 Oct;2(4):249-51.). In this study we explored the JAM-A/F11R expression in MM tumor cells and in patients to determine the potential role of this molecule in the pathogenesis and progression of MM. Methods: The MM cell lines examined were RPMI-8266, U266, and NCI-H929. Human umbilical vein endothelial cells (HUVECs) served as controls. Informed consent was obtained from patients and control subjects. Primary BM tumor cells were enriched to > 95% CD138+ cells by positive selection using anti-CD138 MACS MicroBeads. The CD138-negative fraction was used for outgrowth of confluent EPCs (> 98% vWF/CD133/KDR+). JAM-A mRNA expression was assessed using an microarray gene expression profile, JAM-A probe based real-time PCR, and JAM-A levels in each sample were measure using a standard curve and normalized to GADPH. JAM-A protein levels in MM cell lines and primary tumor cells were measured by flow cytometry and immunofluorescence. For serum studies, peripheral blood was obtained from 25 newly diagnosed MM patients and 8 healthy, age- and sex-matched controls, and JAM-A levels were measured using an ELISA. Statistical analysis was performed using Student's t-test, two-tailed, with P ' .05 considered significant. Results: JAM-A mRNA levels were significantly increased in MM cell lines RPMI-8266, U266, and NCI-H929 compared to HUVECs (U266, P = 3×10-5; RPM1-8266, P = 1×10-6; NC1-H929, P= 5×10-4). The JAM-A mRNA levels were significantly greater in RPMI-8226; P < .04 compared to TNFα-activated HUVECs for 24 hours which is a proangiogenic switch for HUVEC gene expression. The elevated mRNA expression of the JAM-A in MM cell lines was confirmed by immunofluorescence and flow cytometry which showed the presence of both membrane and cytoplasmic JAM-A protein. Microarray analysis of gene expression profiles from 20 patients' corresponding tumor cells and microenvironmental EPCs showed that JAM-A had a higher level of expression in tumor cells versus MM EPC by 12.62 fold, (P=.0000642). Furthermore, JAM-A had a higher level of expression in MM EPC versus normal control EPC by 2.41 fold, (P=.00113) reflecting a complex regulatory role of F11 signaling in MM, similar to breast cancer (Naik, U. et al 2008). JAM-A was also found to be 12.6 fold greater in tumor cells compared to EPCS (P=.0000642). In addition, circulating levels of soluble JAM-A were found to be significantly greater in the serum of MM patients compared to controls (P < .005), with an average 2-fold increase. Serum levels of JAM-A in MM patients also decreased 71% with treatment n=5, P<.05. Conclusion: We show for the first time that JAM-A expression is highly elevated in MM tumor cells and its levels respond to treatment. In addition, MM patients have higher circulating JAM-A levels compared to healthy individuals and circulating JAM-A levels were reduced following treatment, suggesting that JAM-A may serve as a novel biomarker in MM. Current studies in the lab are aimed at correlating these levels with clinical parameters to determine whether JAM-A levels reflect disease severity and response to treatment. Results of these analyses, as well as results of ongoing experiments using JAM-A siRNA and antibody-inhibition approaches to target JAM-A in myeloma tumor and ECs will be presented. Disclosures: No relevant conflicts of interest to declare.

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Heit, John A., Sebastian M. Armasu, Tanya Petterson, David N. Rider, Julie M. Cunningham, and Mariza de Andrade. "Association of Gene-Environment Interactions with Venous Thromboembolism (VTE): A Pathway-Directed Candidate-Gene Case-Control Study." Blood 116, no. 21 (November 19, 2010): 480. http://dx.doi.org/10.1182/blood.v116.21.480.480.

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Abstract Abstract 480 Background: While interaction between Factor V Leiden and other VTE risk exposures (i.e., oral contraceptives, hormone therapy, pregnancy, cancer, minor trauma) compound VTE risk, whether other gene-environment interactions are associated with VTE is largely unknown. Objective: To test gene-environment interactions for an association with VTE. Methods: Cases (n=1488) were Mayo Clinic European-American patients of non-Hispanic ancestry with objectively-diagnosed VTE in the absence of active cancer, venous catheter or antiphospholipid antibodies. Controls (n=1439) were Mayo Clinic outpatients without VTE who were frequency-matched on case age, gender, race, MI/stroke status and state of residence. We selected candidate genes relevant to the anticoagulant, procoagulant, fibrinolytic and innate immunity pathways, focusing on platelet, monocyte, neutrophil and endothelial cell agonists, receptors, ligands, signal transduction and adhesion molecules, granule contents and effectors; plasma proteases and inhibitors; matrix metalloproteases; inflammatory cytokines and receptors; estrogen, progesterone and androgen receptors; co-regulators and enzymes related to estrogen metabolism; important enzymes for catechol, homocysteine, thromboxane A2 and prostacyclin biosynthesis and metabolism; and HMG CoA reductase. For these genes (n=750), we selected all non-synonymous coding single nucleotide polymorphisms (SNPs) with minor allele frequency ≥0.5%; the remaining SNPs were selected using an LD tagging algorithm (Carlson et al. AJHG 2004); 479 ancestry-informative markers were also included (total n=13,241 SNPs). Leukocyte genomic DNA was genotyped using a custom Illumina Infinium iSelect platform, including appropriate controls. We tested all pairwise interactions between 12,483 SNPs (12296 autosomal, 187 chromosome X) that passed quality control and each of seven exposures (ever “stress”[defined as ever hospitalized, ever surgery, ever trauma, ever transfemoral procedure or ever leg paresis], ever surgery, ever neurosurgery, ever orthopedic surgery; and among women, ever pregnant, ≥3 pregnancies and ever oral contraceptives/hormone therapy), adjusted for age, gender, MI/stroke status and state of residence, using logistic regression. False discovery rates (q-value) were calculated to estimate the expected fraction of false positive associations due to multiple statistical tests. Results: The mean ± SD case and control ages were 55.3 ± 16.4 and 56.5 ± 15.9 years, respectively, and 51% were female. Analysis of ancestry-informative markers revealed no evidence of population stratification. Among the seven models, a significant interaction (q≤0.05) was found between ever surgery and two genes located on chromosome 1: USF1 (rs2516840, OR=2.1, p=2.0E-06; q=0.02), and F11R (rs790055 & rs790056; OR∼2.29, p∼4E-06; q=0.02); the two F11R SNPs are in complete linkage dysequilibrium (LD), and the USF1 SNP is in moderate LD with the F11R SNPs (r2∼0.6). USF1 encodes for upstream transcription factor 1 which regulates many genes involved in lipid and glucose homeostasis. F11R encodes for the platelet F11 receptor (JAM [junctional adhesion molecule], a cell adhesion molecule important for platelet adhesion to cytokine-stimulated endothelial cells. Conclusion: Interaction between surgery and SNPs within USF1 and F11R are associated with significantly increased risks for VTE. These potential associations require confirmation in future replication studies. Disclosures: No relevant conflicts of interest to declare.

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23

Barea, J. M., G. Andrade, V. Bianciotto, D. Dowling, S. Lohrke, P. Bonfante, F. O’Gara, and C. Azcon-Aguilar. "Impact on Arbuscular Mycorrhiza Formation ofPseudomonas Strains Used as Inoculants for Biocontrol of Soil-Borne Fungal Plant Pathogens." Applied and Environmental Microbiology 64, no. 6 (June 1, 1998): 2304–7. http://dx.doi.org/10.1128/aem.64.6.2304-2307.1998.

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ABSTRACT The arbuscular mycorrhizal symbiosis, a key component of agroecosystems, was assayed as a rhizosphere biosensor for evaluation of the impact of certain antifungal Pseudomonas inoculants used to control soil-borne plant pathogens. The following threePseudomonas strains were tested: wild-type strain F113, which produces the antifungal compound 2,4-diacetylphloroglucinol (DAPG); strain F113G22, a DAPG-negative mutant of F113; and strain F113(pCU203), a DAPG overproducer. Wild-type strain F113 and mutant strain F113G22 stimulated both mycelial development from Glomus mosseae spores germinating in soil and tomato root colonization. Strain F113(pCU203) did not adversely affectG. mosseae performance. Mycelial development, but not spore germination, is sensitive to 10 μM DAPG, a concentration that might be present in the rhizosphere. The results of scanning electron and confocal microscopy demonstrated that strain F113 and its derivatives adhered to G. mosseae spores independent of the ability to produce DAPG.

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Eiberg, H., L. S. Nielsen, and J. Mohr. "Confirmation of F13A assignment and sequence information concerning F13A-HLA-GLO." Clinical Genetics 26, no. 5 (April 23, 2008): 385–88. http://dx.doi.org/10.1111/j.1399-0004.1984.tb01077.x.

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25

Lewandowska, K., E. Balza, L. Zardi, and L. A. Culp. "Requirement for two different cell-binding domains in fibronectin for neurite extension of neuronal derivative cells." Journal of Cell Science 95, no. 1 (January 1, 1990): 75–83. http://dx.doi.org/10.1242/jcs.95.1.75.

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Some neuron-derived cells, such as neuroblastoma cells, adhere and extend neurites on fibronectin (FN) substrata by processes that can be independent of binding to the Arg-Gly-Asp-Ser sequence (RGDS in FN) and independent of proteoglycan/ganglioside-binding activities of FN. Proteolytic fragments of various FNs have been used in this study to map a new adhesion-promoting domain in FNs that may be neural cell-specific. A thermolysin-generated fragment of human plasma FN (F110 containing the RGDS domain) or the analagous fragment from transformed human cell FN (F120, also containing the alternately spliced extra domain b[EDb]) facilitate RGDS-independent adherence and neurite extension of human neuroblastoma cells and an F11 hybrid neuronal line (by fusion of mouse neuroblastoma cells with rat dorsal root ganglion neurons) as effectively as adherence and neurite extension on intact FN. Since neither F110 nor F120 contains sequences from the alternately spliced IIICS region of FN, neurite-promoting activity in these fragments cannot be ascribed to a recently discovered cell-binding domain in this region. Furthermore, F120 could be cleaved into two subfragments retaining virtually all the sequence of the parent fragment: F35 from the C terminus of F120 containing the RGDS domain, and F90 from the N terminus containing most of the EDb region bordering the thermolysin cleavage site. These neuronal cells could adhere but not extend neurites on substrata coated with either F35 or F90 alone while 3T3 cells could adhere only on F35. Mixtures of F35 and F90 on substrata could reconstitute some, but not nearly all, of the neurite-promoting activity of F120. Therefore, these data identify a new cell-binding domain in common sequences of FNs on the N-terminal side of EDb and demonstrate cooperativity between this RGDS-independent domain and the RGDS-dependent domain for maximal differentiation of these neuron-derived cells. Several possibilities for a receptor directed to this new domain are discussed.

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26

Wada, Satoshi, and Petr Pulpan. "Domain Wall Engineering in Lead-Free Piezoelectric Materials." Key Engineering Materials 421-422 (December 2009): 13–16. http://dx.doi.org/10.4028/www.scientific.net/kem.421-422.13.

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Grain-oriented barium titanate (BaTiO3, BT) ceramics were prepared by a templated grain growth (TGG) method using [110]-oriented BT platelike particles as a template and hydrothermal BT sphere particles with different particle sizes as a matrix. The degree of orientation along the [110] direction, F110, was measured using an X-ray diffraction (XRD) pattern by the Lotgering method. To obtain both a high density and a high F110, the preparation conditions were optimized as functions of matrix particle size, volume fraction of the template to the matrix, and sintering temperature. As for the results, BT grain-oriented ceramics with a high density of more than 96 % were successfully prepared despite various F110 values from 0 to 98 %. Scanning electron microscopy (SEM) revealed that their average grain sizes were always 75 µm despite various F110 values and there were no anisotropic microstructures. These grain-oriented BT ceramics were poled at 100 °C, and their piezoelectric constants d33 was measured. As for the results, the d33 values increased with increasing F110 values, and at around an F110 of 85 %, d33 reached a maximum of 788 pC/N.

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Schwedler, Christian, Guido Heymann, Larisa Bukreeva та Berthold Hoppe. "Association of Genetic Polymorphisms of Fibrinogen, Factor XIII A-Subunit and α2-Antiplasmin with Fibrinogen Levels in Pregnant Women". Life 11, № 12 (3 грудня 2021): 1340. http://dx.doi.org/10.3390/life11121340.

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Fibrinogen synthesis is stimulated by proinflammatory triggers and depends on α-, β- and γ-fibrinogen (FGA, FGB, FGG) genotypes. Constellations of fibrinogen, factor XIII A-subunit (F13A) and α2-antiplasmin (A2AP) genotypes predisposing for dense fibrin gels with high antifibrinolytic capacity (e.g., FGB rs1800790 A-allele carriage in F13A 34Val/Val or A2AP 6Arg/Arg wildtypes) are related with reduced inflammation. As both relationships are likely to influence each other, we tested whether the association of fibrinogen genotypes with fibrinogen levels is influenced by F13A and A2AP genotypes in a population under proinflammatory stress. In total, 639 women were followed during pregnancy (2218 observations). The relationship between fibrinogen genotypes and levels was statistically assessed in univariate and multivariate analyses without and with stratification for F13A Val34Leu and A2AP Arg6Trp. Strong associations with fibrinogen levels could be found for FGB rs1800790G > A, FGA rs2070016T > C and FGG rs1049636T > C. For FGB rs1800790G > A and FGA rs2070016T > C, this relationship significantly depended on F13A Val34Leu and A2AP Arg6Trp genotypes. Specifically, in F13A 34Val/Val wildtypes, carriage of FGB rs1800790A was related to significantly lower fibrinogen levels compared with FGB rs1800790GG wildtypes (p < 0.01). For A2AP 6Arg/Arg wildtypes, a comparable relationship could be found (p < 0.04). As these genotype constellations related to lower fibrinogen levels have previously been shown to be associated with reduced inflammatory activity, these findings suggest that the influence of fibrinogen, F13A and A2AP genotypes on inflammation could affect the control of fibrinogen levels and vice versa.

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Rittenhouse-Olson, Kate. "JAA-F11." Expert Opinion on Biological Therapy 7, no. 7 (July 2007): 923–28. http://dx.doi.org/10.1517/14712598.7.7.923.

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Qin, Yun, Stefan Imobersteg, Alain Blanc, Stephan Frank, Roger Schibli, Martin P. Béhé, and Michal Grzmil. "Evaluation of Actinium-225 Labeled Minigastrin Analogue [225Ac]Ac-DOTA-PP-F11N for Targeted Alpha Particle Therapy." Pharmaceutics 12, no. 11 (November 12, 2020): 1088. http://dx.doi.org/10.3390/pharmaceutics12111088.

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The overexpression of cholecystokinin B receptor (CCKBR) in human cancers led to the development of radiolabeled minigastrin analogues for targeted radionuclide therapy, which aims to deliver cytotoxic radiation specifically to cancer cells. Alpha emitters (e.g., actinium-225) possess high potency in cancer cell-killing and hold promise for the treatment of malignant tumors. In these preclinical studies, we developed and evaluated CCKBR-targeted alpha particle therapy. The cellular uptake and cytotoxic effect of actinium-225 labeled and HPLC-purified minigastrin analogue [225Ac]Ac-PP-F11N were characterized in the human squamous cancer A431 cells transfected with CCKBR. Nude mice bearing A431/CCKBR tumors were used for biodistribution and therapy studies followed by histological analysis and SPECT/CT imaging. In vitro, [225Ac]Ac-PP-F11N showed CCKBR-specific and efficient internalization rate and potent cytotoxicity. The biodistribution studies of [225Ac]Ac-PP-F11N revealed CCKBR-specific uptake in tumors, whereas the therapeutic studies demonstrated dose-dependent inhibition of tumor growth and extended mean survival time, without apparent toxicity. The histological analysis of kidney and stomach indicated no severe adverse effects after [225Ac]Ac-PP-F11N administration. The post-therapy SPECT-CT images with [111In]In-PP-F11N confirmed no CCKBR-positive tumor left in the mice with complete remission. In conclusion, our study demonstrates therapeutic efficacy of [225Ac]Ac-PP-F11N without acute radiotoxicity in CCKBR-positive cancer model.

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30

Muneyyirci-Delale, O., A. Babinska, V. L. Nacharaju, M. Dalloul, and E. Kornecki. "Enhanced levels of F11R receptor (F11R/JAM-1/JAM-A) in PCOS patients." Fertility and Sterility 88 (September 2007): S186. http://dx.doi.org/10.1016/j.fertnstert.2007.07.641.

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31

Abbas, Abdelhamid, John E. McGuire, Delores Crowley, Christine Baysse, Max Dow, and Fergal O'Gara. "The putative permease PhlE of Pseudomonas fluorescens F113 has a role in 2,4-diacetylphloroglucinol resistance and in general stress tolerance." Microbiology 150, no. 7 (July 1, 2004): 2443–50. http://dx.doi.org/10.1099/mic.0.27033-0.

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2,4-Diacetylphloroglucinol (PHL) is the primary determinant of the biological control activity of Pseudomonas fluorescens F113. The operon phlACBD encodes enzymes responsible for PHL biosynthesis from intermediate metabolites. The phlE gene, which is located downstream of the phlACBD operon, encodes a putative permease suggested to be a member of the major facilitator superfamily with 12 transmembrane segments. PhlE has been suggested to function in PHL export. Here the sequencing of the phlE gene from P. fluorescens F113 and the construction of a phlE null mutant, F113-D3, is reported. It is shown that F113-D3 produced less PHL than F113. The ratio of cell-associated to free PHL was not significantly different between the strains, suggesting the existence of alternative transporters for PHL. The phlE mutant was, however, significantly more sensitive to high concentrations of added PHL, implicating PhlE in PHL resistance. Furthermore, the phlE mutant was more susceptible to osmotic, oxidative and heat-shock stresses. Osmotic stress induced rapid degradation of free PHL by the bacteria. Based on these results, we propose that the role of phlE in general stress tolerance is to export toxic intermediates of PHL degradation from the cells.

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Wadia, A. R., and F. D. James. "F110-GE-132: Enhanced Power Through Low-Risk Derivative Technology." Journal of Turbomachinery 123, no. 3 (February 1, 2000): 544–51. http://dx.doi.org/10.1115/1.1378301.

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The F110-GE-132, originally referred to as the F110-GE-129 EFE (Enhanced Fighter Engine), presently undergoing qualification testing, is being offered at two different thrust/inspection levels with a maximum augmented thrust of 34,000 pounds. The EFE has been developed using low-risk derivative engine technology. It features a new increased airflow, high efficiency, three-stage long chord blisk fan, and an advanced radial augmentor that reduces complexity, improves maintainability, and provides increased parts life. The paper first provides a historical background of the F110 engines to relate the heritage of the F110-GE-132. The F110 engine model development roadmap is shown to illustrate the incremental low-risk approach used to provide thrust growth with improved product reliability. A detailed description of the unique power management features of the EFE engine to meet individual customer thrust and life requirements is outlined. The long chord blisk fan design, development, and test results are presented, followed by a description of the radial augmentor and the exhaust nozzle. The EFE engine has successfully completed sea level static and altitude development testing and fan aero mechanical qualification at the AEDC in Tullahoma, Tennessee.

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Valderrama, Ferran, João V. Cordeiro, Sibylle Schleich, Friedrich Frischknecht, and Michael Way. "Vaccinia Virus-Induced Cell Motility Requires F11L-Mediated Inhibition of RhoA Signaling." Science 311, no. 5759 (January 20, 2006): 377–81. http://dx.doi.org/10.1126/science.1122411.

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RhoA signaling plays a critical role in many cellular processes, including cell migration. Here we show that the vaccinia F11L protein interacts directly with RhoA, inhibiting its signaling by blocking the interaction with its downstream effectors Rho-associated kinase (ROCK) and mDia. RNA interference–mediated depletion of F11L during infection resulted in an absence of vaccinia-induced cell motility and inhibition of viral morphogenesis. Disruption of the RhoA binding site in F11L, which resembles that of ROCK, led to an identical phenotype. Thus, inhibition of RhoA signaling is required for both vaccinia morphogenesis and virus-induced cell motility.

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SHIROTA, Minori, Tomoyuki IMADA, Kohei ITO, Hidetaka MURAMATSU, Yasuyuki TAKATA, and Motoo FUJII. "F113 Hydrogen solubility in water." Proceedings of the National Symposium on Power and Energy Systems 2008.13 (2008): 269–70. http://dx.doi.org/10.1299/jsmepes.2008.13.269.

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Jagadeeswaran, Pudur. "RFLP in human F13A gene." Nucleic Acids Research 18, no. 5 (1990): 1317. http://dx.doi.org/10.1093/nar/18.5.1317.

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Kotani, Osamu, Yasushi Suzuki, Shinji Saito, Akira Ainai, Akira Ueno, Takuya Hemmi, Kaori Sano, et al. "Structure-Guided Creation of an Anti-HA Stalk Antibody F11 Derivative That Neutralizes Both F11-Sensitive and -Resistant Influenza A(H1N1)pdm09 Viruses." Viruses 13, no. 9 (August 31, 2021): 1733. http://dx.doi.org/10.3390/v13091733.

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The stalk domain of influenza virus envelope glycoprotein hemagglutinin (HA) constitutes the axis connecting the head and transmembrane domains, and plays pivotal roles in conformational rearrangements of HA for virus infection. Here we characterized molecular interactions between the anti-HA stalk neutralization antibody F11 and influenza A(H1N1)pdm09 HA to understand the structural basis of the actions and modifications of this antibody. In silico structural analyses using a model of the trimeric HA ectodomain indicated that the F11 Fab fragment has physicochemical properties, allowing it to crosslink two HA monomers by binding to a region near the proteolytic cleavage site of the stalk domain. Interestingly, the F11 binding allosterically caused a marked suppression of the structural dynamics of the HA cleavage loop and flanking regions. Structure-guided mutagenesis of the F11 antibody revealed a critical residue in the F11 light chain for the F11-mediated neutralization. Finally, the mutagenesis led to identification of a unique F11 derivative that can neutralize both F11-sensitive and F11-resistant A(H1N1)pdm09 viruses. These results raise the possibility that F11 sterically and physically disturbs proteolytic cleavage of HA for the ordered conformational rearrangements and suggest that in silico guiding experiments can be useful to create anti-HA stalk antibodies with new phenotypes.

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Mellata, Melha, Maryvonne Dho-Moulin, Charles M. Dozois, Roy Curtiss, Peter K. Brown, Pascal Arné, Annie Brée, Clarisse Desautels, and John M. Fairbrother. "Role of Virulence Factors in Resistance of Avian Pathogenic Escherichia coli to Serum and in Pathogenicity." Infection and Immunity 71, no. 1 (January 2003): 536–40. http://dx.doi.org/10.1128/iai.71.1.536-540.2003.

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ABSTRACT In chickens, colibacillosis is caused by avian pathogenic Escherichia coli (APEC) via respiratory tract infection. Many virulence factors, including type 1 (F1A) and P (F11) fimbriae, curli, aerobactin, K1 capsule, and temperature-sensitive hemagglutinin (Tsh) and plasmid DNA regions have been associated with APEC. A strong correlation between serum resistance and virulence has been demonstrated, but roles of virulence factors in serum resistance have not been well elucidated. By using mutants of APEC strains TK3, MT78, and χ7122, which belong to serogroups O1, O2, and O78, respectively, we investigated the role of virulence factors in resistance to serum and pathogenicity in chickens. Our results showed that serum resistance is one of the pathogenicity mechanisms of APEC strains. Virulence factors that increased bacterial resistance to serum and colonization of internal organs of infected chickens were O78 lipopolysaccharide of E. coli χ7122 and the K1 capsule of E. coli MT78. In contrast, curli, type 1, and P fimbriae did not appear to contribute to serum resistance. We also showed that the iss gene, which was previously demonstrated to increase resistance to serum in certain E. coli strains, is located on plasmid pAPEC-1 of E. coli χ7122 but does not play a major role in resistance to serum for strain χ7122.

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Grzmil, Michal, Stefan Imobersteg, Alain Blanc, Stephan Frank, Roger Schibli, and Martin P. Béhé. "Therapeutic Response of CCKBR-Positive Tumors to Combinatory Treatment with Everolimus and the Radiolabeled Minigastrin Analogue [177Lu]Lu-PP-F11N." Pharmaceutics 13, no. 12 (December 15, 2021): 2156. http://dx.doi.org/10.3390/pharmaceutics13122156.

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The inhibition of the mammalian target of rapamycin complex 1 (mTORC1) by everolimus (RAD001) was recently shown to enhance the tumor uptake of radiolabeled minigastrin. In this paper, we investigate if this finding can improve the in vivo therapeutic response to [177Lu]Lu-PP-F11N treatment. The N-terminal DOTA-conjugated gastrin analogue PP-F11N (DOTA-(DGlu)6-Ala-Tyr-Gly-Trp-Nle-Asp-Phe) was used to evaluate treatment efficacy in the human A431/CCKBR xenograft nude mouse model in combination with RAD001. Both RAD001 and [177Lu]Lu-PP-F11N single treatments as well as their combination inhibited tumor growth and increased survival. In concomitantly treated mice, the average tumor size and median survival time were significantly reduced and extended, respectively, as compared to the monotherapies. The histological analysis of kidney and stomach dissected after treatment with RAD001 and [177Lu]Lu-PP-F11N did not indicate significant adverse effects. In conclusion, our study data demonstrate the potential of mTORC1 inhibition to substantially improve the therapeutic efficacy of radiolabeled minigastrin analogues in CCKBR-positive cancers.

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Zisch, A. H., L. D'Alessandri, B. Ranscht, R. Falchetto, K. H. Winterhalter, and L. Vaughan. "Neuronal cell adhesion molecule contactin/F11 binds to tenascin via its immunoglobulin-like domains." Journal of Cell Biology 119, no. 1 (October 1, 1992): 203–13. http://dx.doi.org/10.1083/jcb.119.1.203.

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Adhesive interactions between neurons and extracellular matrix (ECM) play a key role in neuronal pattern formation. The prominent role played by the extracellular matrix protein tenascin/cytotactin in the development of the nervous system, tied to its abundance, led us to speculate that brain may contain yet unidentified tenascin receptors. Here we show that the neuronal cell adhesion molecule contactin/F11, a member of the immunoglobulin(Ig)-superfamily, is a cell surface ligand for tenascin in the nervous system. Through affinity chromatography of membrane glycoproteins from chick brain on tenascin-Sepharose, we isolated a major cell surface ligand of 135 kD which we identified as contactin/F11 by NH2-terminal sequencing. The binding specificity between contactin/F11 and tenascin was demonstrated in solid-phase assays. Binding of immunopurified 125I-labeled contactin/F11 to immobilized tenascin is completely inhibited by the addition of soluble tenascin or contactin/F11, but not by fibronectin. When the fractionated isoforms of tenascin were used as substrates, contactin/F11 bound preferentially to the 190-kD isoform. This isoform differs in having no alternatively spliced fibronectin type III domains. Our results imply that the introduction of these additional domains in some way disrupts the contactin/F11 binding site on tenascin. To localize the binding site on contactin/F11, proteolytic fragments were generated and characterized by NH2-terminal sequencing. The smallest contactin/F11 fragment which binds tenascin is 45 kD and also begins with the contactin/F11 NH2-terminal sequence. This implies that contactin/F11 binds to tenascin through a site within the first three Ig-domains.

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Naik, U. P., Y. H. Ehrlich та E. Kornecki. "Mechanisms of platelet activation by a stimulatory antibody: cross-linking of a novel platelet receptor for monoclonal antibody F11 with the FcγRII receptor". Biochemical Journal 310, № 1 (15 серпня 1995): 155–62. http://dx.doi.org/10.1042/bj3100155.

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The mechanisms by which a stimulatory monoclonal antibody (mAb), called mAb F11, induces granular secretion and aggregation in human platelets have been characterized. Fab fragments of mAb F11, as well as an mAb directed against the platelet Fc gamma RII receptor (mAb IV.3) were found to inhibit mAb F11-induced platelet secretion and aggregation, indicating that the mAb F11 IgG molecule interacts with the Fc gamma RII receptor through its Fc domain and with its own antigen through its Fab domain. The mAb F11 recognized two platelet proteins of 32 and 35 kDa on the platelet membrane surface, as identified by Western blot analysis. We purified both proteins from human platelet membranes using DEAE-Sepharose chromatography followed by mAb F11 affinity chromatography. When added to platelet-rich plasma, the purified proteins dose-dependently inhibited mAb F11-induced platelet aggregation. The purified protein preparation also competitively inhibited the binding of 125I-labelled mAb F11 to intact platelets. The N-terminal 26 amino acid sequences of both the 32 and 35 kDa proteins were identical and contained a single unblocked serine in the N-terminal position. When digested with N-glycanase, the 32 and 35 kDa proteins were converted into a single approximately 29 kDa protein, indicating that these two proteins are derived from the same core protein but differ in their degree of glycosylation. Internal amino acid sequence analysis of the F11 antigen provided information concerning 68 amino acids and suggested two consensus phosphorylation sites for protein kinase C (PKC). The phosphorylation by PKC of the isolated F11 antigen was observed following stimulation by phorbol 12-myristate 13-acetate. Databank analysis of the N-terminal and internal amino acid sequences of the F11 antigen indicated that the N-terminal sequence exhibited the highest degree of similarity to the variable region of the alpha-chain of human T-cell receptors (TCR). In contrast, the F11 internal sequences did not exhibit any similarity to the TCR. Our results demonstrate that the F11 antigen is a novel platelet membrane surface glycoprotein which becomes cross-linked with the Fc gamma RII receptor when platelets are activated by the stimulatory mAb F11. These mechanisms may be relevant to the production of immune thrombocytopenia by platelet-activating antibodies.

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41

Caeiro, J. L. B., E. Parra, A. Gremo, and Ruiz de la Cuestd. "Distribution of F13A Phenotypes in Spain: A Particularly High Frequency of the F13A*2 Allele." Human Heredity 42, no. 4 (1992): 264–68. http://dx.doi.org/10.1159/000154080.

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42

Nörenberg, U., M. Hubert, T. Brümmendorf, A. Tárnok, and F. G. Rathjen. "Characterization of functional domains of the tenascin-R (restrictin) polypeptide: cell attachment site, binding with F11, and enhancement of F11-mediated neurite outgrowth by tenascin-R." Journal of Cell Biology 130, no. 2 (July 15, 1995): 473–84. http://dx.doi.org/10.1083/jcb.130.2.473.

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The extracellular matrix glycoprotein tenascin-R (TN-R) is a multidomain protein implicated in neural cell adhesion. To analyze the structure-function relationship of the different domains of TN-R, several recombinant TN-R fragments were expressed in bacterial cells. Two distinct binding regions were localized on the TN-R polypeptide: a region binding the axon-associated immunoglobulin (Ig)-like F11 protein and a cell attachment site. The binding region of the glycosylphosphatidylinositol (GPI)-anchored F11 was allocated to the second and third fibronectin type III (FNIII)-like domain within TN-R. By using a mutant polypeptide of F11 containing only Ig-like domains, a direct interaction between the Ig-like domains of F11 and FNIII-like domains 2-3 of TN-R was demonstrated. The interaction of TN-R with F11 in in vitro cultures enhanced F11-mediated neurite outgrowth, suggesting that the combined action of F11 and TN-R might be of regulatory influence on axon extension. A cell attachment region was identified in the FNIII-like domain eight of TN-R by domain-specific antibodies and fusion constructs. This site is distinct from the F11 binding site within TN-R.

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43

Chen, Wei, Yongxia Liu, Jinhua Yin, Youtian Deng, Tariq Ali, Ju Zhang, Jia Cheng, Sadeeq ur Rahman, Jian Gao, and Bo Han. "Cloning, Expression, and Immunogenicity of Fimbrial-F17A Subunit Vaccine againstEscherichia coliIsolated from Bovine Mastitis." BioMed Research International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/3248483.

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There is a need to identify and select new promising immunodominant antigens that have the ability to provide protective immunity againstE. colicausing bovine mastitis. Recently we showed thatf17awas found to be the most prevalent and crucial virulent factor among the pathogenicE. coliisolated from bovine mastitis. Here, in this report, the recombinant F17A based subunit vaccine adjuvant with MF59 was tested for immunogenicity againstE. coliin a murine model. The vaccinated mice did not show any abnormal behavioral changes and histopathological lesions after vaccination. The specific antibody level against F17A was significantly higher in MF59-adjuvant-group, and also lasted for longer duration with a significant(P<0.01)production level of IgG1 and IgG2a. Moreover, we noted higher survival rate in mice injected with F17A-MF59-adjuvant group after challenging with the clinicalE. colistrain.Our findings of bacterial clearance test revealed that elimination rate from liver, spleen, and kidney in MF59-adjuvant-group was significantly higher than the control group. Finally, the proportion of CD4+T cells was increased, while CD8+ was decreased in MF59-adjuvant group. In conclusion, the current study reveals the capability of F17A-MF59 as a potential vaccine candidate against pathogenicE. colicausing mastitis in dairy animals.

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44

Wu, Guoyu, Junyang Yi, Ling Liu, Pengcheng Wang, Zhijie Zhang та Zhen Li. "Pseudoginsenoside F11, a Novel Partial PPARγAgonist, Promotes Adiponectin Oligomerization and Secretion in 3T3-L1 Adipocytes". PPAR Research 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/701017.

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PPARγis a nuclear hormone receptor that functions as a master regulator of adipocyte differentiation and development. Full PPARγagonists, such as the thiazolidinediones (TZDs), have been widely used to treat type 2 diabetes. However, they are characterized by undesirable side effects due to their strong agonist activities. Pseudoginsenoside F11 (p-F11) is an ocotillol-type ginsenoside isolated fromPanax quinquefolium L.(American ginseng). In this study, we found that p-F11 activates PPARγwith modest adipogenic activity. In addition, p-F11 promotes adiponectin oligomerization and secretion in 3T3-L1 adipocytes. We also found that p-F11 inhibits obesity-linked phosphorylation of PPARγat Ser-273 by Cdk5. Therefore, p-F11 is a novel partial PPARγagonist, which might have the potential to be developed as a new PPARγ-targeted therapeutics for type 2 diabetes.

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45

Villacieros, Marta, Clare Whelan, Martina Mackova, Jesper Molgaard, María Sánchez-Contreras, Javier Lloret, Daniel Aguirre de Cárcer, et al. "Polychlorinated Biphenyl Rhizoremediation by Pseudomonas fluorescens F113 Derivatives, Using a Sinorhizobium meliloti nod System To Drive bph Gene Expression." Applied and Environmental Microbiology 71, no. 5 (May 2005): 2687–94. http://dx.doi.org/10.1128/aem.71.5.2687-2694.2005.

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ABSTRACT Rhizoremediation of organic chemicals requires high-level expression of biodegradation genes in bacterial strains that are excellent rhizosphere colonizers. Pseudomonas fluorescens F113 is a biocontrol strain that was shown to be an excellent colonizer of numerous plant rhizospheres, including alfalfa. Although a derivative of F113 expressing polychlorinated biphenyl (PCB) biodegradation genes (F113pcb) has been reported previously, this strain shows a low level of bph gene expression, limiting its rhizoremediation potential. Here, a high-level expression system was designed from rhizobial nod gene regulatory relays. Nod promoters were tested in strain F113 by using β-galactosidase transcriptional fusions. This analysis showed that nodbox 4 from Sinorhizobium meliloti has a high level of expression in F113 that is dependent on an intact nodD1 gene. A transcriptional fusion of a nodbox cassette containing the nodD1 gene and nodbox 4 fused to a gfp gene was expressed in the alfalfa rhizosphere. The bph operon from Burkholderia sp. strain LB400 was cloned under the control of the nodbox cassette and was inserted as a single copy into the genome of F113, generating strain F113L::1180. This new genetically modified strain has a high level of BphC activity and grows on biphenyl as a sole carbon and energy source at a growth rate that is more than three times higher than that of F113pcb. Degradation of PCBs 3, 4, 5, 17, and 25 was also much faster in F113L::1180 than in F113pcb. Finally, the modified strain cometabolized PCB congeners present in Delor103 better than strain LB400, the donor of the bph genes used.

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46

Liu, Yonggang, Wenda Shi, Enmin Zhou, Shujie Wang, Shouping Hu, Xuehui Cai, Fulong Rong, et al. "Dynamic Changes in Inflammatory Cytokines in Pigs Infected with Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus." Clinical and Vaccine Immunology 17, no. 9 (July 14, 2010): 1439–45. http://dx.doi.org/10.1128/cvi.00517-09.

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ABSTRACT Porcine reproductive and respiratory syndrome virus (PRRSV) infection induces both humoral and cellular immune responses. In this study, we investigated the changes in cytokine levels in peripheral blood between the highly pathogenic PRRSV HuN4 strain and its derivative strain HuN4-F112 obtained by serial propagation in MARC145 cells to 112 passages. The results demonstrated that pigs infected with HuN4 showed a loss of appetite, decrease in body weight, raised body temperature, and respiratory symptoms, along with interstitial pneumonia lesions. The PRRSV amounts in the pigs infected with HuN4 were 105 to 109 copies/ml in the blood and 1010 to 1011 copies/g in the lung tissues, whereas the virus amounts with HuN4-F112 were 102.15 to 103.13 copies/ml in the blood and 103.0 to 103.6 copies/g in the lungs. Moreover, the levels of interleukin 1 (IL-1), IL-6, tumor necrosis factor alpha (TNF-α), and alpha interferon (IFN-α) in peripheral blood were upregulated 7 days postinoculation with HuN4, which was earlier than in the HuN4-F112 group. Furthermore, cytokine levels in the pigs infected with HuN4 returned to normal on the 21st day postinoculation, while the levels in those infected with HuN4-F112 continued to increase. These results demonstrated that the pigs infected with the highly pathogenic PRRSV HuN4 strain generated earlier and higher levels of inflammatory cytokines, and the results also indicated that HuN4 may aggravate inflammation and damage tissues and organs. The low-pathogenic PRRSV HuN4-F112 strain induced lower levels of inflammatory cytokines, which may enhance the immune responses against the infection.

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47

Mugnai, G., K. Lewandowska, B. Carnemolla, L. Zardi, and L. A. Culp. "Modulation of matrix adhesive responses of human neuroblastoma cells by neighboring sequences in the fibronectins." Journal of Cell Biology 106, no. 3 (March 1, 1988): 931–43. http://dx.doi.org/10.1083/jcb.106.3.931.

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Attachment and neurite extension have been measured when Platt or La-N1 human neuroblastoma cells respond to tissue culture substrata coated with a panel of complementary fragments from the individual chains of human plasma (pFN) or cellular fibronectins (cFN) purified from thermolysin digests. A 110-kD fragment (f110), which contains the Arg-Gly-Asp-Ser sequence (RGDS)-dependent cell-binding domain but no heparin-binding domains and whose sequences are shared in common by both the alpha- and beta-subunits of pFN, facilitated attachment of cells that approached the level observed with either intact pFN or the heparan sulfate-binding platelet factor-4 (PF4). This attachment on f110 was resistant to RGDS-containing peptide in the medium. Neurite outgrowth was also maximal on f110, and half of these neurites were also resistant to soluble RGDS peptide. Treatment of cells with glycosaminoglycan lyases failed to alter these responses on f110. Therefore, there is a second "cell-binding" domain in the sequences represented by f110 that is not RGDS- or heparan sulfate-dependent and that facilitates stable attachment and some neurite outgrowth; this domain appears to be conformation-dependent. Comparisons were also made between two larger fragments generated from the two subunits of pFN-f145 from the alpha-subunit and f155 from the beta-subunit--both of which contain the RGDS-dependent cell-binding domain and the COOH-terminal heparin-binding domain but which differ in the former's containing some IIICS sequence at its COOH terminus and the latter's having an additional type III homology unit. Heparin-binding fragments (with no RGDS activity) of f29 and f38, derived from f145 or f155 of pFN, respectively, and having the same differences in sequence, were also compared with f44 + 47 having the "extra domain" characteristic of cFN. Attachment on f145 was slightly sensitive to soluble RGDS peptide; attachment on f155 was much more sensitive. There were also differences in the percentage of cells with neurites on f145 vs. f155 but neurites on either fragment were completely sensitive to RGDS peptide. Mixing of f29, f38, or PF4 with f110 could not reconstitute the activities demonstrated in f145 or f155, demonstrating that covalently linked sequences are critical in modulating these responses. However, mixing of f44 + 47 from cFN with f110 from pFN increased the sensitivity to RGDS peptide.(ABSTRACT TRUNCATED AT 400 WORDS)

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48

Xu, Caiyan, Jianjun Zhai, and Yujing Fu. "lncRNA F11-AS1 Suppressed Cervical Cancer Biological Activities by Vitro Study." Journal of Biomaterials and Tissue Engineering 9, no. 11 (November 1, 2019): 1512–19. http://dx.doi.org/10.1166/jbt.2019.2165.

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Objection: The purpose of this work was to discuss the effects and relative mechanisms of F11-AS1 in cervical cancer treatment by vitro study. Methods: 20 pairs of cervical carcinoma and adjacent normal tissue were collected and measured pathology and F11-AS1 expression by HE and HIS staining. Measuring F11-AS1 expression in difference cell lines and cell groups by RT-qPCR assay. Transfection F11-AS1 in Hela cells, evaluating hela cell biological including proliferation, apoptosis, invasion and migration by MTT, flow cytometry, transwell and wound healing assay. PTEN, p-PI3K and AKT proteins expression were evaluated by WB assay, and p-PI3K nuclear volume were measured by cellular immunofluorescence assay. Results: F11-AS1 level of cancer tissues were significantly down-regulation with state increasing by ISH assay (P < 0.01, respectively). After transfection with F11-AS1, the Hela cell proliferation rate was significantly down-regulation with apoptosis significantly increasing (P < 0.05); The invasion Hela cell number and wound healing rate were significantly depressed with F11-AS1 transfection (P < 0.05). By WB assay, PTEN protein expression was significantly increasing, and p-PI3K and AKT proteins expression were significantly inhibited (P < 0.05). By cellular immunofluorescence assay, p-PI3K nuclear volume of pcDNA3.1/F11-AS1 group was significantly depressed (P < 0.05). Conclusion: lncRNA F11-AS1 suppressed cervical cancer biological activities by regulation PTEN/p-PI3K/AKT pathway in vitro study.

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49

Song, Fang, and Fengshuang Li. "Long Non-Coding RNA F11-Antisense 1 (F11-AS1) Suppresses Ovarian Cancer Biological Activity by Regulating Phosphatase and Tensin Homolog Deleted on Chromosome Ten (PTEN)." Journal of Biomaterials and Tissue Engineering 11, no. 9 (September 1, 2021): 1752–59. http://dx.doi.org/10.1166/jbt.2021.2632.

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Aim: To discuss F11-AS1’s effects and mechanisms in ovarian cancer development. Methods: Evaluating F11-AS1 expression by ISH assay and F11-AS1 mRNA level in difference cell lines by RT-qPCR assay. Using MTT, flow cytometry, transwell and wound healing assay to evaluate SKOV3 cell proliferation, cell apoptosis, invasion and migration. And using WB assay to measure PTEN, p-PI3K, AKT, P53 and MMP-9 proteins expressions. Results: F11-AS1 was significantly down-regulation with stage increasing in cancer tissues (P <0.01, respectively). With F11-AS1 transfection, the SKOV3 cell proliferation rate was significantly depressed with cell apoptosis and G1 phase rate significantly increasing (P <0.001, respectively). And then, invasion cell number and wound healing rate of lncRNA group which transfected with F11-AS1 significantly down-regulation (P <0.001). By WB assay, PTEN and P53 proteins expressions significantly up-regulation and p-PI3K, AKT and MMP-9 proteins expressions were significantly down-regulation (P <0.001). Conclusion: F11-AS1 depresses ovarian cancer biological activity by regulating PTEN by vitro study.

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50

Mora Ferrera, José Carlos, Francisco Javier Núñez Sánchez, Francisco Ignacio Martínez Cabrera, Pablo Rodríguez Sánchez, and Luís Suárez Moreno-Arrones. "Comparación de las demandas de carrera Futbol 7 vs. Fútbol 11 en jugadores jóvenes de fútbol (Running requirements comparison between Football 7 and Football 11 with youth soccer players)." Retos, no. 26 (March 6, 2015): 149–52. http://dx.doi.org/10.47197/retos.v0i26.34421.

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El objetivo de este estudio fue comparar las demandas físicas que exigen dos modalidades de juego distintas en fútbol a jugadores jóvenes (Fútbol 7 (F7) vs. Fútbol 11 (F11)). 26 sujetos de entre 12 y 15 años fueron valorados durante la primera parte de 8 partidos (4 de F7 y 4 de F11). Los datos se midieron con GPS de 1 Hz. Los principales resultados fueron: 1) el rendimiento de carrera fue superior (en términos absolutos) cuanto mayor edad, tanto en F7 como en F11, 2) en general, para el mismo grupo de edad, el F11 supuso mayor demanda física que el F7, 3) en la misma categoría, hubo mayor demanda física en el grupo de mayor nivel (sólo en F11). En síntesis, los resultados mostraron una mayor demanda física del F11 frente al F7 en la mayoría de las comparaciones realizadas. Dicha demanda de carrera también aumentó conforme lo hacía la categoría según la edad, sobre todo se encontraron diferencias entre Infantil B (infantiles de primer año en la categoría) y Alevín. Todo esto podría indicar que el cambio de superficie de juego que se da al pasar de categoría alevín a categoría infantil (y por tanto, de F7 a F11) podría ser demasiado drástico, ya que en muy pocos meses los jugadores cambian de categoría. Por tanto, hemos llegado a la conclusión de que podría ser conveniente establecer un terreno de juego de dimensiones intermedias entre F7 y F11 en la categoría infantil que haga el cambio de dimensiones más progresivo.Palabras Clave: fútbol, fútbol 7, demandas de carrera, GPS, jóvenes.Abstract: The aim of this study is to compare the running requirements of playing football in two different modes with youth players (Football 7 (F7) vs. Football 11 (F11)). 26 individuals (12-15 years old) were measured during the first half of 8 matches (4 of F7 and 4 of F11). Data was collected with 1 Hz GPS. The main results were: 1) running performance was higher (in absolute terms) in the oldest players, both in F7 and F11, 2) generally, within the same age group, F11 was physically more demanding than F7, 3) within the same category, the highest level group obtained the greatest physical exertion (only F11). To sum up, results showed that F11 necessitated greater physical exertion than F7 in the majority of comparisons. This running demands also rose according the age and, above all, differences were found between «Infantil B» (under-13, playing F11 according to the rules for the first time) and «Alevín» (under-12). These discoveries may indicate that the change of the dimensions of the pitch from «Alevín» to «Infantil» (therefore, from F7 size to F11 size) may be too drastic because players change from one category to the other in only a few months. We therefore suggest that it may be convenient for the «Infantil» players (under-13 and under-14) to establish a pitch with intermediate dimensions between F7 size and F11 size. This would make the step from one size to the other more progressive in terms of physical exertion.Keywords: football, football 7, running requirements, GPS, youth players.

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