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1

Köster, B., and M. Strand. "Schistosoma mansoni: immunolocalization of two different fucose-containing carbohydrate epitopes." Parasitology 108, no. 4 (May 1994): 433–46. http://dx.doi.org/10.1017/s0031182000075995.

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SUMMARYWe have used two monoclonal antibodies, 128C3/3 and 504B1, to immunolocalize their carbohydrate epitopes in different developmental stages of Schistosoma mansoni. Both epitopes contain fucose: mAb 128C3/3, as we have shown previously, recognizes fucose in a novel, possibly internal linkage (Levery et al. 1992) while mAb 504B1, as we show here, bound to the Lex epitope, which contains fucose α1 → 3 linked to N-acetyl-glucosamine. The tissue expression of these epitopes was strikingly different and both elicit an immune response in infected hosts. The mAb 128C3/3-defined epitope was exposed on the surface of all larval stages but not on adult worms; however, it was found in the excretory system of adult worms of both sexes. In contrast, surface expression of the Lex epitope was initiated after the transformation of cercariae to schistosomula and was maintained throughout the adult life in both sexes.
2

Creson, Jennifer R., Andy A. Lin, Qun Li, David F. Broad, Margo R. Roberts, and Stephen J. Anderson. "The Mode and Duration of Anti-CD28 Costimulation Determine Resistance to Infection by Macrophage-Tropic Strains of Human Immunodeficiency Virus Type 1 In Vitro." Journal of Virology 73, no. 11 (November 1, 1999): 9337–47. http://dx.doi.org/10.1128/jvi.73.11.9337-9347.1999.

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ABSTRACT We have investigated the ability of anti-CD28 antibody costimulation to induce resistance to macrophage (M)-tropic strains of human immunodeficiency virus type 1 (HIV-1) in vitro. Our results confirm the observations of Levine et al. (15) that stimulation of CD4 T cells with anti-CD3/anti-CD28 antibodies coimmobilized on magnetic beads renders the cells resistant to infection by M-tropic strains of HIV-1. The resistance was strongest when the beads were left in the cultures throughout the experiment. In contrast, stimulation of CD4 T cells with the same antibodies immobilized on the surface of plastic culture dishes failed to induce resistance and resulted in high levels of p24 production. This was true even if the cells were passaged continuously on freshly coated plates. If the beads were removed after initial stimulation, p24 production increased over time and produced a result intermediate to the other forms of stimulation. For beads-in, beads-out, and one-time plate stimulated cultures, resistance to infection correlated with down-regulation of CCR5 expression at the cell surface and with increased production of β-chemokines. However, cultures of CD4 T cells continuously passaged on anti-CD3/anti-CD28-coated plates produced large amounts of p24 despite decreased levels of CCR5 expression and increasing production of β-chemokines. Expression of the T-cell activation markers CD25 and CD69 and production of gamma interferon further supported the differences in plate versus bead stimulation. Our results explain the apparent contradiction between the ability of anti-CD28 antibody costimulation to induce resistance to HIV infection when presented on magnetic beads and the increased ability to recover virus from the cells of HIV-positive donors who are on highly active antiretroviral therapy when cells are stimulated by anti-CD3/anti-CD28 immobilized on plastic dishes.
3

Bagashev, Asen, Elena Sotillo, Glendon Wu, and Andrei Thomas-Tikhonenko. "The Importance of CD19 Exon 2 for Surface Localization: Closing the Ig-like Loop." Blood 126, no. 23 (December 3, 2015): 3433. http://dx.doi.org/10.1182/blood.v126.23.3433.3433.

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Abstract Background: CD19 is a near-universal surface marker of B-cell malignancies. Therefore, it is regarded as a target of choice for various immunotherapies, such as bi-specific T-cell engagers and chimeric antigen receptor-armed T-cells. Although the latter have proven remarkably effective in treating B-cell acute lymphoblastic leukemia (B-ALL), relapses caused by the loss of the CD19 surface epitopes are emerging as a major reason for treatment failure (Maude et al, 2014). However, the molecular mechanisms of epitope loss remain incompletely characterized. Recently, we have identified a novel alternatively spliced CD19 isoform lacking exon2 (Δex2 CD19) (Sotillo et al 2015). Although exon 2 encodes a single conserved N-linked glycosylation site (Asn-86) and two conserved cysteine residues (Cys-38 and Cys-97) responsible for the formation of a disulfide bond (Zhou et al 1991), the function and subcellular localization of the Δex2 isoform remained unknown. Our aim was to identify specific amino acids within exon 2 that are responsible for proper CD19 surface expression. Methods: CD19-null (ΔCD19) derivatives of Nalm6 and 697 B-ALL cell lines were generated using the CRISPR/Cas9 approach. We then reconstituted them with full-length and Δex2 CD19 isoforms, expressed either on their own or as CD19-GFP fusions. Additionally, CD19 N-terminus mutations (ΔSP [no signal peptide], N86A, C97A and N86A/C97A) were introduced in full-length CD19. Transduced cells were analyzed by flow cytometry, confocal microscopy, and western blotting. Glycosylation of the mutants was verified using treatment with swainsonine (Golgi glycosylation inhibitor) and an in vitro de-glycosylation assay. Results: As expected, deletion of the N-terminal signal peptide responsible for the endoplasmic reticulum translocation led to impaired surface expression. Surprisingly, deletion of exon 2 sequences had a similar effect: although up to 10% of Δex2 CD19 was found on the plasma membrane (where it enhanced pre-B-cell receptor signaling), the remainder was largely cytosolic. Furthermore, while the N86A substitution in full-length CD19 did not significantly affect its surface localization, substituting Cys-97 with Ala fully recapitulated the Δex2 cytosolic phenotype. In fact, the C97A mutant appeared to be stuck in the ER and never reach Golgi, since its electrophoretic mobility was not affected by swainsonine. In contrast, its glycosylation in ER was unperturbed, as evidenced by in vitro de-glycosylation assays. Conclusion: The immunoglobulin-like loop connecting Cys-38 and Cys-97 of CD19 is required for its plasma membrane localization. One possible mechanism is the N-termini-mediated interaction with CD81, which is known to be needed to transport CD19 to the cell surface (Matsumoto et al 1993). Maude SL, Frey, N, Shaw, PA, Aplenc R, Barrett DM, Bunin NJ, Chew A, Gonzalez VE, Zheng Z, Lacey SF, Mahnke YD, Melenhorst JJ, Rheingold SR, Shen A, Teachey DT, Levine BL, June CH, Porter DL, and Grupp SA. Chimeric antigen receptor T cells for sustained remissions in leukemia. N Engl J Med 2014 371:1507-1517. Sotillo E, Barrett D, Bagashev A, Black K, Lanauze C, Oldridge D, Sussman R, Harrington C, Chung EY, Hofmann TJ, Maude SL, Martinez NM, Raman P, Ruella M, Allman D, Jacoby E, Fry T, Barash Y, Lynch KW, Mackall C, Maris J, Grupp SA, and Thomas-Tikhonenko A. Alternative splicing of CD19 mRNA in leukemias escaping CART-19 immunotherapy eliminates the cognate epitope andcontributes to treatment failure. 2015 AACR Annual Meeting, Philadelphia. Zhou LJ, Ord DC, Hughes AL and Tedder TF, Structure and domain organization of the CD19 antigen of human, mouse, and guinea pig B lymphocytes. Conservation of the extensive cytoplasmic domain. J Immunol. 1991 147(4):1424-32 Matsumoto AK, Martin DR, Carter RH, Klickstein LB, Ahearn JM, and Fearon DT Functional dissection of the CD21/CD19/TAPA-1/Leu-13 complex of B lymphocytes. J Exp Med. 1993 178(4):1407-17. Disclosures No relevant conflicts of interest to declare.
4

Labroussaa, Fabien, Vincent Baby, Sébastien Rodrigue, and Carole Lartigue. "La transplantation de génomes." médecine/sciences 35, no. 10 (October 2019): 761–70. http://dx.doi.org/10.1051/medsci/2019154.

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Le développement de la génomique synthétique (GS) a permis l’élaboration d’outils et de méthodes innovantes permettant la synthèse, l’assemblage et la modification génétique précise de chromosomes bactériens complets. La raison principale de ce succès, ayant abouti à la création de la première cellule synthétique quasi-minimale JCVI-syn3.0, est l’utilisation de la levure Saccharomyces cerevisiae comme hôte temporaire d’accueil et de modification de ces génomes. Cependant, une autre technique a joué un rôle considérable dans le succès retentissant de ces travaux : la transplantation de génomes bactériens (TG). Cette technique, encore mal comprise, permet d’installer des génomes complets naturels ou synthétiques dans un contexte cellulaire favorable à leur expression et donner la vie. Une meilleure compréhension du processus de TG permettrait d’élargir l’ensemble des techniques de GS, appliquées actuellement quasi exclusivement à l’étude des mycoplasmes, à de nombreuses autres bactéries d’intérêt, y compris des bactéries génétiquement non-modifiables à ce jour.
5

RAHAMIMOFF, HANNAH, XIAOYAN REN, CHAVA KIMCHI-SARFATY, SURESH AMBUDKAR, and JUDITH KASIR. "NCX1 Surface Expression." Annals of the New York Academy of Sciences 976, no. 1 (January 24, 2006): 176–86. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04739.x.

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6

Käfer, G., A. Willer, W. D. Ludwig, A. Krämer, R. Hehlmann, and J. Hastka. "Intracellular expression of CD61 precedes surface expression." Annals of Hematology 78, no. 10 (October 21, 1999): 472–74. http://dx.doi.org/10.1007/s002770050601.

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7

Kanematsu, Takashi, Makoto Fujii, Hiroto Tanaka, Hisanori Umebayashi, and Masato Hirata. "Surface Expression of GABAA Receptors." Journal of Oral Biosciences 52, no. 4 (January 2010): 322–29. http://dx.doi.org/10.1016/s1349-0079(10)80012-x.

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8

Dunbar, Andrew, Min Lu, Mirko Farina, Young Park, Julie Yang, Dongjoo Kim, Abdul Karzai, et al. "Increased Interleukin-8 (IL8)-CXCR2 Signaling Promotes Progression of Bone Marrow Fibrosis in Myeloproliferative Neoplasms." Blood 136, Supplement 1 (November 5, 2020): 6–7. http://dx.doi.org/10.1182/blood-2020-138843.

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Introduction: Elevated pro-inflammatory cytokines are a hallmark feature of myeloproliferative neoplasms (MPNs). The pro-inflammatory cytokine interleukin-8 (IL8) is increased in patients with myelofibrosis (MF) and correlates with adverse outcome, including overall survival. Previously, the Levine/Fang labs identified increased IL8 secretion from individual CD34+ stem cells in a subset of MF patients. The role of IL8 and its cognate receptors CXCR1/2 in MF pathogenesis has not been delineated. Methods: Single-cell cytokine assays were performed on isolated CD34+ cells from 60 clinically annotated MPN patients (20 MF, 20 PV, 20 ET) using a previously described micro-chip platform (Kleppe et al, Can Disc 2013). 10 healthy donors (CD34+ cells from hip replacements) were used as controls. Integrated RNA-Seq and Assay for Transposase-Accessible Chromatin followed by next-generation sequencing (ATAC-Seq) was performed on CD34+ cells from MPN patients with and without expanded IL8 secreting clones for gene expression/chromatin accessibility analysis. To model the role of IL8-CXCR2 on fibrosis in vivo, the human MPLW515L transplant model (hMPLW515L) of MF was used. Specifically, wild-type (WT) murine bone marrow (Creneg-Cxcr2f/f; Cxcr2WT) or marrow lacking the CXCR2 receptor (VavCre-Cxcr2f/f; Cxcr2KO)were retrovirally infected with MSCV-hMPLW515L-IRES-GFP and transplanted into lethally irradiated WT recipient mice and monitored for disease. Blood counts, chimerism, and flow cytometry were assayed. Moribund mice were sacrificed and assayed for grade reticulin fibrosis and overall survival. Results: Single-cell cytokine assays confirmed an increased proportion of IL8-secreting CD34+ cells in MF patients (40%) in comparison to other MPN sub-types (10% PV/0% ET) (Figure 1A). MF patients with expanded IL8 secreting clones (defined as >50% of total CD34+ cells) had increased leukocytosis (p<0.0001), larger spleen sizes (p=0.0004), greater prevalence of constitutional symptoms (p=0.0084), and higher-grade reticulin fibrosis in marrow (Figure 1B) in comparison to MF patients without prevalent IL8 clones. IHC confirmed increased IL8 expression in marrow biopsies from 8/15 MF patients in comparison to 0/4 normal controls (Figure 1C), and high IL8 expression was also observed in MF splenic megakaryocytes (MKs) as well as in splenic stromal/endothelial cells not seen in normal spleen (Figure 1D). Integrated RNA-Seq/ATAC-Seq analysis of IL8-high MF patients confirmed up-regulation of IL8-CXCR2 signaling and enrichment in pro-inflammatory pathways (i.e TNFa, NFkB, etc) by GSEA, as well as increased expression/accessibility of pro-inflammatory genes S100A8 and S100A9-previously implicated in fibrosis development. Flow analysis of IL8-high MF CD34+ cells revealed enhanced surface expression of CXCR2 and its analog CXCR1, such that MF was characterized by increased IL8 ligand and receptor expression (Figure 1E) and coincided with enhanced NFkB pathway activity (Figure 1F). Consistent with this, colony forming assays of cultured MF CD34+ cells revealed enhanced colony output when cultured with IL8 compared to WT CD34+ cells-an effect ameliorated by co-treatment with the CXCR1/2 antagonist Reparixin (Figure 1G). In vivo, hMPLW515L adoptive transplant with Cxcr2KO hematopoietic donor cells demonstrated improved leukocytosis, thrombocytosis (Figure 2A) and splenomegaly in comparison to Cxcr2WT hMPLW515L recipient mice. Pathologic analysis revealed a reduction in reticulin fibrosis in bone marrow (Figure 2B) and spleen, translating into an improvement in overall survival (Figure 2C). Notably, a significant reduction in dysplastic MKs-a hallmark feature of MF-was also observed in Cxcr2KO hMPLW515L mice (Figure 2D) supporting a role for CXCR2 signaling in MK proliferation. Conclusion: IL8 secreting clones are associated with increased symptom severity and fibrosis grade in MF. Gene expression of MF CD34+ IL8 secreting clones shows up-regulation of inflammatory genes S100A8/A9, implicated in myofibroblast proliferation. Cxcr2 KO abrogates fibrosis formation and prolongs survival in the hMPLW515L model, and CXCR1/2 inhibition impairs colony forming capacity of MF CD34+ cells. These data suggest pharmacologic inhibition of this pathway should be investigated as potential therapy in MF and in PV/ET patients at high risk of fibrotic transformation. Disclosures Fan: IsoPlexis: Current Employment, Current equity holder in private company; Singleron Biotechnologies: Current Employment, Current equity holder in private company. Levine:Morphosys: Consultancy; Prelude Therapeutics: Research Funding; Qiagen: Current equity holder in publicly-traded company, Membership on an entity's Board of Directors or advisory committees; Gilead: Honoraria; Loxo: Current equity holder in private company, Membership on an entity's Board of Directors or advisory committees; Novartis: Consultancy; Amgen: Honoraria; Astellas: Consultancy; Imago: Current equity holder in private company, Membership on an entity's Board of Directors or advisory committees; C4 Therapeutics: Current equity holder in private company, Membership on an entity's Board of Directors or advisory committees; Isoplexis: Current equity holder in private company, Membership on an entity's Board of Directors or advisory committees; Celgene: Consultancy, Honoraria, Research Funding; Roche: Consultancy, Honoraria, Research Funding; Lilly: Consultancy, Honoraria; Janssen: Consultancy. Hoffman:Protagonist: Consultancy; Abbvie: Membership on an entity's Board of Directors or advisory committees; Dompe: Research Funding; Novartis: Membership on an entity's Board of Directors or advisory committees; Forbius: Consultancy.
9

Swamynathan, Shivalingappa K. "Ocular Surface Development and Gene Expression." Journal of Ophthalmology 2013 (2013): 1–22. http://dx.doi.org/10.1155/2013/103947.

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The ocular surface—a continuous epithelial surface with regional specializations including the surface and glandular epithelia of the cornea, conjunctiva, and lacrimal and meibomian glands connected by the overlying tear film—plays a central role in vision. Molecular and cellular events involved in embryonic development, postnatal maturation, and maintenance of the ocular surface are precisely regulated at the level of gene expression by a well-coordinated network of transcription factors. A thorough appreciation of the biological characteristics of the ocular surface in terms of its gene expression profiles and their regulation provides us with a valuable insight into the pathophysiology of various blinding disorders that disrupt the normal development, maturation, and/or maintenance of the ocular surface. This paper summarizes the current status of our knowledge related to the ocular surface development and gene expression and the contribution of different transcription factors to this process.
10

Pope, Kevin O., Adriana C. Ocampo, Gary L. Kinsland, and Randy Smith. "Surface expression of the Chicxulub crater." Geology 24, no. 6 (1996): 527. http://dx.doi.org/10.1130/0091-7613(1996)024<0527:seotcc>2.3.co;2.

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11

Yurchenko, Vyacheslav, Tatiana Pushkarsky, Jian-Hua Li, Wei Wei Dai, Barbara Sherry, and Michael Bukrinsky. "Regulation of CD147 Cell Surface Expression." Journal of Biological Chemistry 280, no. 17 (January 25, 2005): 17013–19. http://dx.doi.org/10.1074/jbc.m412851200.

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12

Benziane, Boubacar, Sylvie Demaretz, Nadia Defontaine, Nancy Zaarour, Lydie Cheval, Soline Bourgeois, Christophe Klein, et al. "NKCC2 Surface Expression in Mammalian Cells." Journal of Biological Chemistry 282, no. 46 (September 11, 2007): 33817–30. http://dx.doi.org/10.1074/jbc.m700195200.

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Apical bumetanide-sensitive Na+-K+-2Cl- co-transporter, termed NKCC2, is the major salt transport pathway in kidney thick ascending limb. NKCC2 surface expression is subject to regulation by intracellular protein trafficking. However, the protein partners involved in the intracellular trafficking of NKCC2 remain unknown. Moreover, studies aimed at under-standing the post-translational regulation of NKCC2 have been hampered by the difficulty to express NKCC2 protein in mammalian cells. Here we were able to express NKCC2 protein in renal epithelial cells by tagging its N-terminal domain. To gain insights into the regulation of NKCC2 trafficking, we screened for interaction partners of NKCC2 with the yeast two-hybrid system, using the C-terminal tail of NKCC2 as bait. Aldolase B was identified as a dominant and novel interacting protein. Real time PCR on renal microdissected tubules demonstrated the expression of aldolase B in the thick ascending limb. Co-immunoprecipitation and co-immunolocalization experiments confirmed NKCC2-aldolase interaction in renal cells. Biotinylation assays showed that aldolase co-expression reduces NKCC2 surface expression. In the presence of aldolase substrate, fructose 1,6-bisphosphate, aldolase binding was disrupted, and aldolase co-expression had no further effect on the cell surface level of NKCC2. Finally, functional studies demonstrated that aldolase-induced down-regulation of NKCC2 at the plasma membrane was associated with a decrease in its transport activity. In summary, we identified aldolase B as a novel NKCC2 binding partner that plays a key role in the modulation of NKCC2 surface expression, thereby revealing a new regulatory mechanism governing the co-transporter intracellular trafficking. Furthermore, NKCC2 protein expression in mammalian cells and its regulation by protein-protein interactions, described here, may open new and important avenues in studying the cell biology and post-transcriptional regulation of the co-transporter.
13

Valk, Elke, Christopher E. Rudd, and Helga Schneider. "CTLA-4 trafficking and surface expression." Trends in Immunology 29, no. 6 (June 2008): 272–79. http://dx.doi.org/10.1016/j.it.2008.02.011.

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14

Ackerman, Margaret E., Cecile Chalouni, Michael M. Schmidt, Vivek V. Raman, Gerd Ritter, Lloyd J. Old, Ira Mellman, and K. Dane Wittrup. "A33 antigen displays persistent surface expression." Cancer Immunology, Immunotherapy 57, no. 7 (January 31, 2008): 1017–27. http://dx.doi.org/10.1007/s00262-007-0433-x.

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15

Holmes, Kevin L., and Herbert C. Morse. "Murine hematopoietic cell surface antigen expression." Immunology Today 9, no. 11 (January 1988): 344–50. http://dx.doi.org/10.1016/0167-5699(88)91335-7.

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16

Sakimoto, Tohru, Jun Shoji, Hitoshi Kanno, and Mitsuru Sawa. "Gelatinase Expression in Ocular Surface Disorders." Japanese Journal of Ophthalmology 48, no. 1 (January 1, 2004): 17–22. http://dx.doi.org/10.1007/s10384-003-0022-2.

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17

FUSI, F. M., and R. A. BRONSON. "Sperm Surface Fibronectin Expression Following Capacitation." Journal of Andrology 13, no. 1 (January 2, 1992): 28–35. http://dx.doi.org/10.1002/j.1939-4640.1992.tb01623.x.

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ABSTRACT: The Arg‐Gly‐Asp (RGD) amino acid sequence plays a role in many cell‐to‐cell and cell‐to‐matrix adhesion systems, as a recognition sequence for cell membrane receptors termed integrins. Receptors of the VLA subfamily of integrins recognize fibronectin, laminin, and collagen. Given the authors' findings that fibronectin‐derived, RGD‐containing peptides competitively inhibit sperm‐oolemmal adhesion and penetration in both heterologous (human‐hamster) and homologous (hamster‐hamster) gamete interactions, the expression of fibronectin on the surface of fresh, capacitated, and acrosome‐reacted human spermatozoa was studied. The majority of fresh spermatozoa did not display fibronectin on their plasma membrane (0 to 16% positive), as demonstrated by the lack of binding of both monoclonal and polyclonal anti‐fibronectin antibodies. In contrast, a significantly greater proportion of spermatozoa (varying between 18% to 100% for different donors) incubated overnight under capacitating conditions reacted with anti‐fibronectin antibodies. The induction of an acrosome reaction with progesterone did not alter the proportion of sperm displaying fibronectin or its distribution on the sperm surface. A physiologic role of fibronectin in sperm‐oolemmal interaction was suggested by the effects of anti‐fibronectin antibodies on sperm oolemmal adhesion and penetration of hamster eggs by human spermatozoa, which were both significantly reduced (P < 0.001).
18

Niisato, Naomi. "A Regulatory Mechanism of ENaC Surface Expression." MEMBRANE 43, no. 5 (2018): 206–10. http://dx.doi.org/10.5360/membrane.43.206.

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19

Jiang, Yue, Sandeepa Dey, and Hiroaki Matsunami. "Calreticulin: Roles in Cell-Surface Protein Expression." Membranes 4, no. 3 (September 16, 2014): 630–41. http://dx.doi.org/10.3390/membranes4030630.

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20

Thebault, Stéphanie, R. Todd Alexander, Wouter M. Tiel Groenestege, Joost G. Hoenderop, and René J. Bindels. "EGF Increases TRPM6 Activity and Surface Expression." Journal of the American Society of Nephrology 20, no. 1 (December 10, 2008): 78–85. http://dx.doi.org/10.1681/asn.2008030327.

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21

Schneider, G. B., H. Perinpanayagam, M. Clegg, R. Zaharias, D. Seabold, J. Keller, and C. Stanford. "Implant Surface Roughness Affects Osteoblast Gene Expression." Journal of Dental Research 82, no. 5 (May 2003): 372–76. http://dx.doi.org/10.1177/154405910308200509.

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The transcription factor Cbfa1 regulates osteoblast differentiation and expression of genes necessary for the development of a mineralized phenotype. The purpose of this study was to determine if Cbfa1 and BSPII gene expression are influenced by implant surface microtopography. Osteoblasts were cultured on 600-grit (grooved) or sandblasted (roughened) cpTi implant discs. Mineralization was evaluated by Alizarin-Red-S staining. Real Time PCR was used for quantitative analysis of Cbfa1 and BSPII gene expression. Enhanced mineralization was seen in osteoblasts grown on roughened implant surfaces relative to tissue culture plastic. Real Time PCR showed significant (P < 0.05) increases in Cbfa1 gene expression in cells grown on roughened, as compared with grooved, implant surfaces. BSPII gene expression was also increased on rough surfaces in the UMR cells, but was reduced in the rat calvarial osteoblast cultures. These results suggest that osteoblast gene expression and mineralization are affected by roughened implant surface microtopographies during osseointegration of dental implants.
22

Toro, Carlos A., and Sebastian Brauchi. "Modulating the surface expression of cold receptors." Temperature 2, no. 2 (March 16, 2015): 160–62. http://dx.doi.org/10.1080/23328940.2015.1017087.

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23

Stringer, James R., and Scott P. Keely. "Genetics of Surface Antigen Expression inPneumocystis carinii." Infection and Immunity 69, no. 2 (February 1, 2001): 627–39. http://dx.doi.org/10.1128/iai.69.2.627-639.2001.

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ABSTRACT This article reviews the molecular genetic data pertaining to the major surface glycoprotein (MSG) gene family of Pneumocystis carinii and its role in surface variation and compares this fungal system to antigenic variation systems in the protozoanTrypanosoma brucei and the bacteriaBorrelia spp.
24

Zhang, Lian, Karyn Foster, Qiuju Li, and Jeffrey R. Martens. "S-acylation regulates Kv1.5 channel surface expression." American Journal of Physiology-Cell Physiology 293, no. 1 (July 2007): C152—C161. http://dx.doi.org/10.1152/ajpcell.00480.2006.

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The number of ion channels expressed on the cell surface shapes the complex electrical response of excitable cells. An imbalance in the ratio of inward and outward conducting channels is unfavorable and often detrimental. For example, over- or underexpression of voltage-gated K+ (Kv) channels can be cytotoxic and in some cases lead to disease. In this study, we demonstrated a novel role for S-acylation in Kv1.5 cell surface expression. In transfected fibroblasts, biochemical evidence showed that Kv1.5 is posttranslationally modified on both the NH2 and COOH termini via hydroxylamine-sensitive thioester bonds. Pharmacological inhibition of S-acylation, but not myristoylation, significantly decreased Kv1.5 expression and resulted in accumulation of channel protein in intracellular compartments and targeting for degradation. Channel protein degradation was rescued by treatment with proteasome inhibitors. Time course experiments revealed that S-acylation occurred in the biosynthetic pathway of nascent channel protein and showed that newly synthesized Kv1.5 protein, but not protein expressed on the cell surface, is sensitive to inhibitors of thioacylation. Sensitivity to inhibitors of S-acylation was governed by COOH-terminal, but not NH2-terminal, cysteines. Surprisingly, although intracellular cysteines were required for S-acylation, mutation of these residues resulted in an increase in Kv1.5 cell surface channel expression, suggesting that screening of free cysteines by fatty acylation is an important regulatory step in the quality control pathway. Together, these results show that S-acylation can regulate steady-state expression of Kv1.5.
25

Murayama, Yuichi, Katashi Fukao, Atsuo Noguchi, and Osamu Takenaka. "Epitope Expression on Primate Lymphocyte Surface Antigens." Journal of Medical Primatology 15, no. 3 (June 1986): 215–26. http://dx.doi.org/10.1111/j.1600-0684.1986.tb00290.x.

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26

König, R., G. Ashwell, and J. A. Hanover. "Glycosylation of CD4. Tunicamycin inhibits surface expression." Journal of Biological Chemistry 263, no. 19 (July 1988): 9502–7. http://dx.doi.org/10.1016/s0021-9258(19)76570-3.

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27

Shur, Barry D. "Expression and function of cell surface galactosyltransferase." Biochimica et Biophysica Acta (BBA) - Reviews on Biomembranes 988, no. 3 (December 1989): 389–409. http://dx.doi.org/10.1016/0304-4157(89)90012-9.

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28

Wang, Zhaomin, Weijuan Qu, and Anand Asundi. "A simplified expression for aspheric surface fitting." Optik 140 (July 2017): 291–98. http://dx.doi.org/10.1016/j.ijleo.2017.02.094.

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29

Dunphy, Cherie H., Lorenzo M. Galindo, and William S. Velasquez. "Multiple Myeloma with Monoclonal Surface Immunoglobulin Expression." Acta Cytologica 40, no. 2 (1996): 358–62. http://dx.doi.org/10.1159/000333768.

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30

Breitling, Frank, Stefan Dübel, Thomas Seehaus, Iris Klewinghaus, and Melvyn Little. "A surface expression vector for antibody screening." Gene 104, no. 2 (August 1991): 147–53. http://dx.doi.org/10.1016/0378-1119(91)90244-6.

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31

Adler, Emily, Paulette Mhawech-Fauceglia, Simon A. Gayther, and Kate Lawrenson. "PAX8 expression in ovarian surface epithelial cells." Human Pathology 46, no. 7 (July 2015): 948–56. http://dx.doi.org/10.1016/j.humpath.2015.03.017.

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32

Deriy, Lucy V., Julie Chor, and Larry L. Thomas. "Surface Expression of Lactoferrin by Resting Neutrophils." Biochemical and Biophysical Research Communications 275, no. 1 (August 2000): 241–46. http://dx.doi.org/10.1006/bbrc.2000.3284.

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33

Hassan, Sheref E., Mikhail Bekarev, Mimi Y. Kim, Juan Lin, Sajida Piperdi, Richard Gorlick, and David S. Geller. "Cell surface receptor expression patterns in osteosarcoma." Cancer 118, no. 3 (July 12, 2011): 740–49. http://dx.doi.org/10.1002/cncr.26339.

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34

Park, Minha, and Andrea J. Tenner. "Glycosylation stabilizes cell surface expression of C1qRp." Immunopharmacology 49, no. 1-2 (August 2000): 40. http://dx.doi.org/10.1016/s0162-3109(00)80112-5.

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35

Beerepoot, Pieter, Vincent M. Lam, and Ali Salahpour. "Measurement of G protein-coupled receptor surface expression." Journal of Receptors and Signal Transduction 33, no. 3 (April 4, 2013): 162–65. http://dx.doi.org/10.3109/10799893.2013.781625.

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36

Hui, Chen. "The Aesthetic Expression of Ecological Architectural Surface Material." Applied Mechanics and Materials 409-410 (September 2013): 482–85. http://dx.doi.org/10.4028/www.scientific.net/amm.409-410.482.

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As the external physical manifestation of the architecture, the material characteristics of the ecological building surface is that it is the most intuitive external carrier of its communication with people. On the premise of meeting the demand of energy efficiency, Ecological building should also produce a surface material expression form which resonates with peoples aesthetic needs, to achieve its unique aesthetic value.
37

Merriam, Daniel F. "Surface expression of buried geologic features in Kansas." Transactions of the Kansas Academy of Science 108, no. 3 & 4 (October 2005): 121–28. http://dx.doi.org/10.1660/0022-8443(2005)108[0121:seobgf]2.0.co;2.

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38

Hashimoto, Minoru, and Daisuke Morooka. "Robotic Facial Expression Using a Curved Surface Display." Journal of Robotics and Mechatronics 18, no. 4 (August 20, 2006): 504–10. http://dx.doi.org/10.20965/jrm.2006.p0504.

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We propose robotic facial expression using a curved surface display. An image of the robot’s face is displayed on a curved screen to form a facial expression easily compared to other mechanical facial expression. The curved surface gives the face a three-dimensional effect due to not possible using a plane image. The curved surface display consists of a domed screen, a fish-eye lens, and a projector. The face robot has a neck to move the head. We detail the domed display, compensation for image distortion, and the drawing of shadow images indicating the direction of a light source. The facial expression is animated and the head moves using the neck conducted. Experiments confirmed the effectiveness of our proposal.
39

Roshchevsky, M. P., S. L. Chudorodova, and I. M. Roshchevskaya. "Expression of atrial depolarization on the body surface." Doklady Biological Sciences 412, no. 1 (February 2007): 15–17. http://dx.doi.org/10.1134/s001249660701005x.

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40

Worapamorn, W., H. Li, H. R. Haase, Z. Pujic, A. A. Girjes, and P. M. Bartold. "Cell Surface Proteoglycan Expression by Human Periodontal Cells." Connective Tissue Research 41, no. 1 (January 2000): 57–68. http://dx.doi.org/10.3109/03008200009005642.

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41

Manganas, Louis N., and James S. Trimmer. "Subunit Composition Determines Kv1 Potassium Channel Surface Expression." Journal of Biological Chemistry 275, no. 38 (July 13, 2000): 29685–93. http://dx.doi.org/10.1074/jbc.m005010200.

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42

Gustavsson, Martin, Madhu Nair Muraleedharan та Gen Larsson. "Surface Expression of ω-Transaminase in Escherichia coli". Applied and Environmental Microbiology 80, № 7 (31 січня 2014): 2293–98. http://dx.doi.org/10.1128/aem.03678-13.

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ABSTRACTChiral amines are important for the chemical and pharmaceutical industries, and there is rapidly growing interest to use transaminases for their synthesis. Since the cost of the enzyme is an important factor for process economy, the use of whole-cell biocatalysts is attractive, since expensive purification and immobilization steps can be avoided. Display of the protein on the cell surface provides a possible way to reduce the mass transfer limitations of such biocatalysts. However, transaminases need to dimerize in order to become active, and furthermore, they require the cofactor pyridoxal phosphate; consequently, successful transaminase surface expression has not been reported thus far. In this work, we produced anArthrobacter citreusω-transaminase inEscherichia coliusing a surface display vector based on the autotransporteradhesininvolved indiffuseadherence (AIDA-I), which has previously been used for display of dimeric proteins. The correct localization of the transaminase in theE. coliouter membrane and its orientation toward the cell exterior were verified. Furthermore, transaminase activity was detected exclusively in the outer membrane protein fraction, showing that successful dimerization had occurred. The transaminase was found to be present in both full-length and proteolytically degraded forms. The removal of this proteolysis is considered to be the main obstacle to achieving sufficient whole-cell transaminase activity.
43

Dhar, Animesh, and Pankaj Ganguly. "Altered expression of platelet surface glycoproteins during storage." British Journal of Haematology 70, no. 1 (September 1988): 71–75. http://dx.doi.org/10.1111/j.1365-2141.1988.tb02436.x.

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44

Huang, Ling C., Daniele Jean, Rita J. Proske, Rose Y. Reins, and Alison M. McDermott. "Ocular Surface Expression andIn VitroActivity of Antimicrobial Peptides." Current Eye Research 32, no. 7-8 (January 2007): 595–609. http://dx.doi.org/10.1080/02713680701446653.

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45

Dean, Douglas C., Thomas M. Birkenmeier, Glenn D. Rosen, and Steven J. Weintraub. "Expression of Fibronectin and Its Cell Surface Receptors." American Review of Respiratory Disease 144, no. 3_pt_2 (September 1991): S25—S28. http://dx.doi.org/10.1164/ajrccm/144.3_pt_2.s25.

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46

Brohée, D., P. Cauchie, and P. Nève. "Surface Membrane Immunoglobulin Expression in Chronic Lymphocytic Leukemia." Acta Haematologica 92, no. 1 (1994): 50–51. http://dx.doi.org/10.1159/000204140.

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47

Yano, Ken, and Koichi Harada. "A Facial Expression Parameterization by Elastic Surface Model." International Journal of Computer Games Technology 2009 (2009): 1–11. http://dx.doi.org/10.1155/2009/397938.

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We introduce a novel parameterization of facial expressions by using elastic surface model. The elastic surface model has been used as a deformation tool especially for nonrigid organic objects. The parameter of expressions is either retrieved from existing articulated face models or obtained indirectly by manipulating facial muscles. The obtained parameter can be applied on target face models dissimilar to the source model to create novel expressions. Due to the limited number of control points, the animation data created using the parameterization require less storage size without affecting the range of deformation it provides. The proposed method can be utilized in many ways: (1) creating a novel facial expression from scratch, (2) parameterizing existing articulation data, (3) parameterizing indirectly by muscle construction, and (4) providing a new animation data format which requires less storage.
48

Cockbill, Louisa. "Optical estimation of the expression of surface molecules." Scilight 2017, no. 16 (October 9, 2017): 160009. http://dx.doi.org/10.1063/1.5008994.

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49

García, M., S. H. Kleven, and M. Garcia. "Expression of Mycoplasma gallisepticum F-Strain Surface Epitope." Avian Diseases 38, no. 3 (July 1994): 494. http://dx.doi.org/10.2307/1592070.

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50

Alves, Luiz Filipe de A., Bruno F. Fernandes, Julia V. Burnier, José J. Mansure, Shawn Maloney, Alexandre N. Odashiro, Emilia Antecka, Dominique F. De Souza, and Miguel N. Burnier. "Expression of SIRT1 in Ocular Surface Squamous Neoplasia." Cornea 31, no. 7 (July 2012): 817–19. http://dx.doi.org/10.1097/ico.0b013e31823f7857.

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