Relevant bibliographies by topics / CD93 signaling

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Academic literature on the topic 'CD93 signaling'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "CD93 signaling"

1

Barbera, Stefano, Luisa Raucci, Roberta Lugano, Gian Marco Tosi, Anna Dimberg, Annalisa Santucci, Federico Galvagni, and Maurizio Orlandini. "CD93 Signaling via Rho Proteins Drives Cytoskeletal Remodeling in Spreading Endothelial Cells." International Journal of Molecular Sciences 22, no. 22 (November 17, 2021): 12417. http://dx.doi.org/10.3390/ijms222212417.

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During angiogenesis, cell adhesion molecules expressed on the endothelial cell surface promote the growth and survival of newly forming vessels. Hence, elucidation of the signaling pathways activated by cell-to-matrix adhesion may assist in the discovery of new targets to be used in antiangiogenic therapy. In proliferating endothelial cells, the single-pass transmembrane glycoprotein CD93 has recently emerged as an important endothelial cell adhesion molecule regulating vascular maturation. In this study, we unveil a signaling pathway triggered by CD93 that regulates actin cytoskeletal dynamics responsible of endothelial cell adhesion. We show that the Src-dependent phosphorylation of CD93 and the adaptor protein Cbl leads to the recruitment of Crk, which works as a downstream integrator in the CD93-mediated signaling. Moreover, confocal microscopy analysis of FRET-based biosensors shows that CD93 drives the coordinated activation of Rac1 and RhoA at the cell edge of spreading cells, thus promoting the establishment of cell polarity and adhesion required for cell motility.
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Riether, Carsten, Ramin Radpour, Chantal L. Bachmann, Christian M. Schürch, Miroslav Arambasic, Gabriela M. Baerlocher, and Adrian F. Ochsenbein. "CD93-Signaling Regulates Self-Renewal and Proliferation of Chronic Myeloid Leukemia Stem Cells in Mice and Humans and Might be a Promising Target for Treatment." Blood 134, Supplement_1 (November 13, 2019): 187. http://dx.doi.org/10.1182/blood-2019-127864.

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Background: The introduction of BCR/ABL-specific tyrosine kinase inhibitors (TKIs) more than two decades ago revolutionized chronic myelogenous leukemia (CML) therapy. The majority of CML patients treated with TKIs obtain durable cytogenetic and molecular responses. However, only a subgroup of these patients can successfully discontinue TKI therapy and maintain a treatment-free remission (Laneuville et al. 2011). TKI-resistant leukemia stem cells (LSCs) persist in the majority of patients at low levels over a prolonged period. These quiescent, self-renewing LSCs in the BM are the major cause of relapse after drug discontinuation (Holyoake et al, 2017). The selective elimination of LSCs requires the definition of unique signaling pathways that promote self-renewal of LSCs but not of normal HSCs. Based on the documented expression of CD93 on LSCs (Kinstrie et al, 2015), the aim of the present study was to investigate the role of the cell surface receptor CD93 in the regulation of self-renewal of human and murine CML LSCs and its contribution to disease development and progression. Methods and Results: We found CD93 expression on LSCs and leukemia progenitor cells but not on more differentiated leukemia granulocytes in a murine retroviral lineage-negative Sca-1+ c-kit+ (LSK) transduction/transplantation CML model. Next-generation sequencing analysis revealed that Cd93-/- LSCs have a silenced gene expression signature particularly in genes involved in the regulation of gene expression, stem cell maintenance and proliferation. Out of the 1120 genes differentially expressed between BL/6 and Cd93-/- LSCs, 1108 genes were down-regulated. In contrast, naïve BL/6 and Cd93-/- hematopoietic stem cells (HSCs) did not display a dysregulation in these pathways. Functionally, CD93-deficiency in LSCs resulted in impaired self-renewal, reduced LSC frequencies in vitro (at least by a factor of 100, P<0.001) and in the incompetence to induce and propagate CML in mice. To study whether CD93-signaling in LSCs relies on ligand-binding to the extracellular domain of CD93, we generated an extracellular domain deletion mutant of CD93 (mCd93intra). Comparable to transduction with full-length mCd93, the expression of Cd93intra restored colony formation of Cd93-/- LSCs in vitro, suggesting that the maintenance of LSC self-renewal is independent of ligand-binding to the extracellular domain of CD93. Furthermore, analysis of the sub-cellular localization of CD93 in CML cells using a lentiviral expression vector encoding for AcGFP1-N1-Cd93 demonstrated nuclear localization of the CD93 intracellular domain (ICD). SCY1 like pseudokinase 1 (SCYL1), a regulator of gene transcription, directly interacts with the highly charged juxta membrane domain of the cytoplasmic tail of CD93 (Bohlson et al, 2005). Silencing of Scyl1 significantly reduced colony formation of BL/6 but not Cd93-/- LSCs in vitro suggesting that the ICD of CD93 regulates gene transcription via Scyl1 in CML LSCs. To discover compounds that affect LSC function similarly as genetic CD93 blockade, we performed a compound screen using the FDA approved drug library V2. The antiemetic agent metoclopramide, which is widely used in clinical routine to reduce nausea in cancer patients, was one very promising candidate identified in the screen. Metoclopramide treatment reduced clonogenic potential of CD93-competent LSCs to comparable levels as CD93-deficient LSCs in vitro without further affecting colony formation of CD93-deficient LSCs. Analysis of LSCs from newly diagnosed CML patients similarly demonstrated that CD93-signaling induces the expression of genes associated with proliferation and stemness, resulting in an increased clonogenic potential in vitro. In addition, colony formation and re-plating capacity in semisolid cultures of human CD34+CD38- LSCs was significantly impaired by metoclopramide at a pharmacological concentration of 0.1mM compared to control treatment. Conclusions: Overall, these results indicate that CD93-siganling is an important regulator of stemness and proliferation of human and murine CML LSCs. Furthermore, this study identifies expression of CD93 by LSCs as promising novel target for the treatment of CML. Disclosures Baerlocher: Novartis: Research Funding.
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Carroll, Virginia A., Mark K. Lafferty, Luigi Marchionni, Joseph L. Bryant, Robert C. Gallo, and Alfredo Garzino-Demo. "Expression of HIV-1 matrix protein p17 and association with B-cell lymphoma in HIV-1 transgenic mice." Proceedings of the National Academy of Sciences 113, no. 46 (October 31, 2016): 13168–73. http://dx.doi.org/10.1073/pnas.1615258113.

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HIV-1 infection is associated with increased risk for B-cell lymphomas. How HIV infection promotes the development of lymphoma is unclear, but it may involve chronic B-cell activation, inflammation, and/or impaired immunity, possibly leading to a loss of control of oncogenic viruses and reduced tumor immunosurveillance. We hypothesized that HIV structural proteins may contribute to lymphomagenesis directly, because they can persist long term in lymph nodes in the absence of viral replication. The HIV-1 transgenic mouse Tg26 carries a noninfectious HIV-1 provirus lacking part of the gag-pol region, thus constituting a model for studying the effects of viral products in pathogenesis. Approximately 15% of Tg26 mice spontaneously develop leukemia/lymphoma. We investigated which viral proteins are associated with the development of leukemia/lymphoma in the Tg26 mouse model, and performed microarray analysis on RNA from spleen and lymph nodes to identify potential mechanisms of lymphomagenesis. Of the viral proteins examined, only expression of HIV-1 matrix protein p17 was associated with leukemia/lymphoma development and was highly expressed in bone marrow before disease. The tumor cells resembled pro-B cells, and were CD19+IgM−IgD−CD93+CD43+CD21−CD23−VpreB+CXCR4+. Consistent with the pro-B-cell stage of B-cell development, microarray analysis revealed enrichment of transcripts, including Rag1, Rag2, CD93, Vpreb1, Vpreb3, and Igll1. We confirmed RAG1 expression in Tg26 tumors, and hypothesized that HIV-1 matrix protein p17 may directly induce RAG1 in B cells. Stimulation of human activated B cells with p17 enhanced RAG1 expression in three of seven donors, suggesting that intracellular signaling by p17 may lead to genomic instability and transformation.
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Hsu, Hui-Chen, Jennie A. Hamilton, Qi Wu, PingAr Yang, Bao Luo, Shutao Xie, Shanrun Liu, Jun Li, and John D. Mountz. "IL-17 receptor A signaling impedes NF-κB p50/p50 repressor and subverts B-cell anergy in BXD2 mice." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 210.7. http://dx.doi.org/10.4049/jimmunol.196.supp.210.7.

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Abstract B-cell fate decision checkpoint 2 at the transitional T2 stage represents a critical checkpoint defect in the development of autoimmune disease. We have found that there is a failure of anergy induction in the CD93+IgM+CD23+ transitional T2 B cells in the spleen of lupus prone BXD2 mice, which is associated with B-cell tolerance loss to anti-IgM or TLR7 in vitro. Interestingly, there was an enhanced BXD2-Il17ra−/− T2 B cell anergy phenotype in vivo, which is associated with a strong B cell anergic response to BCR or TLR7 stimulation in vitro. Abnormal survival of T2 B cells is thought to be regulated through a strong BAFF-R signaling. Surprisingly, despite normal expression of BAFF-R, BlyS cannot reverse the anergic response of BXD2-Il17ra−/− B cells to BCR stimulation. Analysis of the expression of IL-17RA in the B-cell subsets in BXD2 mice shows that only T2 and germinal center (PNA+Fas+) B cells, but not T1, T3 or mature (CD93−) B cells express surface IL-17RA. Single cell analysis of T2 B cells reveals the co-expression of Il17ra with B-cell activation gene, Bclxl. The strong anergic phenotype of BXD2-Il17ra−/− mouse B cells is associated with a dramatically enhanced nuclear expression of NF-κB1 (p50) and down-modulation of NF-κB phospho-p65. Our results suggest that, in BXD2-Il17ra−/− B cells, the anergy phenotype is established at the T2 stage. In these B cells, the stimulus-specific transcription repressor p50/p50 homodimer may act as a master transcriptional regulator to counteract pro-activation/survival NF-κB signaling provided by other major B-cell stimulators to enforce B cell anergy. Reagents that can promote the NF-κB p50/p50 repressome complex may be a novel strategy to enhance B-cell tolerance for autoimmunity.
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Riether, Carsten, Ramin Radpour, Nils M. Kallen, Damian T. Bürgin, Chantal Bachmann, Christian M. Schürch, Ursina Lüthi, et al. "Metoclopramide treatment blocks CD93-signaling-mediated self-renewal of chronic myeloid leukemia stem cells." Cell Reports 34, no. 4 (January 2021): 108663. http://dx.doi.org/10.1016/j.celrep.2020.108663.

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Zhang, Hui, Zhaohui Zhu, and Gary Meadows. "Effects of chronic alcohol consumption on B cells in B16BL6 melanoma-bearing mice (66.24)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 66.24. http://dx.doi.org/10.4049/jimmunol.186.supp.66.24.

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Abstract We previously found that chronic alcohol consumption inhibits CD8+ T cell immunity in B16BL6 melanoma-bearing mice and also decreases their survival. Recent reports indicate that lack of B cells, especially mature B cells, compromises CD8+ T cell anti-tumor immunity. It is unknown if alcohol consumption affects B cells in tumor-bearing hosts. Herein, we studied the effects of chronic alcohol consumption on B cell phenotypes in B16BL6 melanoma-bearing mice. Alcohol consumption did not alter the number of B cells in the bone marrow (BM), spleen or lymph nodes, but decreased B cells in the peritoneal cavity (PC) and blood. Notably, the B cell number decreased 3-4 fold in blood. The percentage of CD19+IgMhiIgDlo immature B cells slightly increased in the BM. Alcohol decreased marginal zone B cells and increased CD23-CD93+ immature B cells, and did not alter follicular B cells in the spleen. The percentage of CD19+CD5+ cells increased in the PC and CD19+CD5- cells decreased. The percentage of CD21+CD23-CD19+ B cells increased 2-fold in blood while CD19+CD23+ cells decreased. Alcohol consumption altered the gene expression of sphingosine-1-phosphate (S1P) receptor-1 (SIPR1) and S1P lyase. Collectively, these data indicate that alcohol decreases mature B cells in the blood and PC by impairing B cell circulation in melanoma-bearing mice. Altered S1P/S1PR1 signaling could contribute to impaired B cell circulation.
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Mountz, John D., Jennie Ann Hamilton, Qi Wu, PingAr Yang, Bao Luo, Shanrun Liu, Jun Li, and Hui-Chen Hsu. "Endogenous dsRNA and dsDNA sensing is increased in transitional B cells in BXD2 autoimmune-prone mice." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 47.2. http://dx.doi.org/10.4049/jimmunol.196.supp.47.2.

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Abstract Enhanced nucleic acid-sensing (NS) pathways has been associated with development of autoimmune disease. Increased type I IFN signaling is identified in lupus prone BXD2 mouse B cells and there is a predominant production of autoantibodies against RNA binding autoantigens in BXD2 mice. Determination of the expression of Usp18 and Oasl2 in early CD93+ transitional B cells (T1 and T2) revealed a surprising finding that early transitional B cell exhibited elevated type I IFN signature gene expression, compared to CD93− mature B cells. Consistent with this, there is also elevated expression of NS pathway genes in early transitional B cells. The most highly expressed were the dsRNA sensing Rig1 and transcription factors Irf3 and Irf7, which were expressed at higher levels compared to pDCs. Interestingly, although Usp18 and Oasl2 levels were undetectable in BXD2-Ifnar−/− transitional B cells, dsRNA sensing gene expression were highly expressed suggesting an IFNAR-independent up-regulation of dsRNA NS pathway in transitional B cells. There was lower expression of Mda5 and Pkr5, and genes involved in DNA sensing including Zbp1 and Irf9. Stimulation of B cells with a RIG1 agonist, poly(I:C)-LMW/LyoVec leads to significantly elevated induction of NS pathway genes in both WT and IFNAR deficient transitional B cells from BXD2 mice. These results suggest that transitional B cells have an intrinsic enhanced nucleic acid-sensing pathway, allowing them to rapidly react to nucleic acid stimulation. Dysregulation of this pathway as a result of apoptotic cell clearance defects can act together with type I IFN stimulation to lead to survival and maturation of B cells that by-pass tolerance checkpoint 2 and produce anti-nucleic acid autoantibodies in lupus.
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Sanchez-Aguilera, Abel, Jose Cancelas, and David A. Williams. "RhoH-Deficient Mice Show Altered B Cell Populations In Vivo." Blood 110, no. 11 (November 16, 2007): 2307. http://dx.doi.org/10.1182/blood.v110.11.2307.2307.

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Abstract RhoH is a GTPase-deficient, hematopoietic-specific member of the family of Rho GTPases (Li et al, 2002). RhoH has been described as regulating proliferation and engraftment of hematopoietic progenitor cells (Gu et al, 2005) and integrin-mediated adhesion in T cells (Cherry et al, 2004). Additionally, RhoH plays a critical role in T-cell development and T-cell receptor signaling (Gu et al, 2006; Dorn et al, 2007). However, the potential role of RhoH in the differentiation and biological functions of B cells are unknown. To answer these questions, we analyzed the B-cell phenotype of RhoH−/− mice and the in vitro properties of RhoH-deficient splenic B cells compared to their wild-type counterparts. RhoH−/− mice showed increased B-cell numbers in the bone marrow, mainly due to an increase in the number of pro-B, pre-B and immature B cells. In the spleen, lymph nodes and peripheral blood, RhoH−/− mice showed a significant decrease in the number of follicular (B-2) cells (B220+ CD93– IgDhigh CD21low). The number of splenic marginal zone B cells (B220+ CD93– IgDlow CD21high), plasma cells (CD93– CD38+ CD138+) in bone marrow and spleen, and B-1 cells (IgM+ CD5+) in peritoneal cavity were not significantly different from those in wild-type animals. These alterations have functional significance, since the serum concentrations of IgM and IgG1 were significantly lower in RhoH−/− mice. However, splenic B cells isolated from RhoH−/− mice did not show any significant differences in their in vitro activation by anti-IgM, CD40 ligation or IL-4 stimulation, nor did they differ in their proliferative response to lipopolysaccharide. In vitro migration of RhoH-deficient B cells in response to CXCL12 or CXCL13 was similar to that of wild-type B cells. Given the important role of RhoH in signal transduction downstream the T cell receptor, we investigated the possible role of RhoH in B cell receptor signaling. Although total splenic B cells from RhoH−/− mice showed markedly increased phosphorylation of SYK and ERK after anti-IgM stimulation compared to wild-type B cells, sorted populations of splenic B-2 and marginal zone B cells from RhoH−/− and wild-type animals did not differ in the activation of these kinases, suggesting that the observed difference can be attributed to the different cellular composition of the B cell compartment (i.e. B-2 vs marginal zone B cells) in RhoH−/− mice. These data imply that the phenotype observed in RhoH−/− mice may not reflect an intrinsic defect in B cells but may be attributed to crosstalk between B cells and other hematopoietic cell populations. Composition of B cell subsets in wild-type and RhoH−/− mice (total cell number ×106, ± standard deviation, N=9) Bone marrow Spleen (*) indicates p<0.05; (**), p<0.01; (***), p<0.005 RhoH+/+ RhoH−/− RhoH+/+ RhoH−/− total B cells 7.8±1.8 11.0±2.4 (**) total B cells 31.7±10.1 25.4±8.8 pro-B 0.12±0.03 0.15±0.04 (*) transitional 8.7±1.2 8.6±2.8 pre-B 2.6±0.6 3.8±0.8 (***) B-2 11.6±4.1 7.6±2.5 (*) immature 1.5±0.4 2.1±0.5 (*) marginal 3.2±1.1 3.9±1.6 mature 1.4±0.7 1.7±0.9
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Marsay, Katherine S., Sarah Greaves, Harsha Mahabaleshwar, Charmaine Min Ho, Henry Roehl, Peter N. Monk, Tom J. Carney, and Lynda J. Partridge. "Tetraspanin Cd9b and Cxcl12a/Cxcr4b have a synergistic effect on the control of collective cell migration." PLOS ONE 16, no. 11 (November 30, 2021): e0260372. http://dx.doi.org/10.1371/journal.pone.0260372.

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Collective cell migration is essential for embryonic development and homeostatic processes. During zebrafish development, the posterior lateral line primordium (pLLP) navigates along the embryo flank by collective cell migration. The chemokine receptors, Cxcr4b and Cxcr7b, as well as their cognate ligand, Cxcl12a, are essential for this process. We corroborate that knockdown of the zebrafish cd9 tetraspanin orthologue, cd9b, results in mild pLL abnormalities. Through generation of CRISPR and TALEN mutants, we show that cd9a and cd9b function partially redundantly in pLLP migration, which is delayed in the cd9b single and cd9a; cd9b double mutants. This delay led to a transient reduction in neuromast numbers. Loss of both Cd9a and Cd9b sensitized embryos to reduced Cxcr4b and Cxcl12a levels. Together these results provide evidence that Cd9 modulates collective cell migration of the pLLP during zebrafish development. One interpretation of these observations is that Cd9 contributes to more effective chemokine signalling.
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Aaron, Tonya, and David R. Fooksman. "Tumor Necrosis Factor Alpha inhibits humoral immunity by regulating the antibody secreting cell bone marrow niche." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 96.02. http://dx.doi.org/10.4049/jimmunol.206.supp.96.02.

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Abstract Humoral immunity is a critical component of the immune memory, and its longevity is partly dependent on the survival of antibody-secreting cells (ASC). Previous studies have shown that several types of infections can deplete pre-existing antibody titers, but the exact mechanism of this process is unclear. Most, if not all, forms of infection induce inflammation including Tumor Necrosis Factor Alpha (TNFa). Here we show that TNFa-mediated inflammation depletes pre-existing antibody titers by limiting ASC retention in the bone marrow (BM) survival niche. Acute recombinant TNFa (rTNFa) treatment induces ASC egress from the BM into the blood and limits engraftment of adoptively transferred ASCs into the BM of recipient mice. To determine if the TNFa-mediated ASC egress from the BM was cell-intrinsic or –extrinsic, we generated BM chimeras with wild-type and TNFa receptor knockout mice. We found that TNFa signaling through TNFa receptor 1 in non-hematopoietic cells induces ASC egress from the BM in a cell-extrinsic manner. Treatment with rTNFa did not induce ASC death in the BM, but it increased glucose uptake and expression of CXCR4, a receptor involved in ASC retention in the BM. In contrast, mobilized ASCs in the blood had reduced glucose uptake, CD98 expression, and CD93 expression suggesting that ASC metabolism is highly dependent on the BM niche. Our findings demonstrate that inflammation alters ASC physiology in both cell-intrinsic and extrinsic manners, leading to reduced antibody titers and long-term immune memory.
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Dissertations / Theses on the topic "CD93 signaling"

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Barbera, Stefano. "The C-type lectin CD93 in physiological and pathological angiogenesis." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1193440.

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Formation of blood vessels is required for development, growth and healing. Although quiescent, endothelial cells (ECs) store a potent proliferative and invasive potential that, upon the appropriate stimuli, is unleashed and gives rise to neovascularization phenomena. Disease progression of cancer and neovascular age-related macular degeneration (nAMD) strongly depends on angiogenesis. In cancer, tumor cells are able to stimulate ECs to become angiogenic and form new blood vessels that allow them to fulfill their tendency to grow and escape the site of the primary tumor. In nAMD, instead, inflammation and drusen deposition induce a strong damage to the retinal pigment epithelium (RPE), which in response to the damage triggers abnormal vessel formation that directly causes disease progression and consequent vision loss. In light of the role that angiogenesis plays in these diseases, targeting blood vessels with anti-angiogenic drugs has always been an appealing concept. However, due to the partial failure of anti-angiogenic therapies in the treatment of such diseases, it has become crucial to find alternative strategies that rely on targeting new molecules in a way to show great efficacy with minimal toxic effects. CD93 is a transmembrane glycoprotein that has been shown to have a prevalent role in controlling EC function, such as cell adhesion and migration. In this work, we investigated the molecular pathways behind the function of CD93 as regulator of EC adhesion and migration, showing that CD93 regulates actin dynamics via the small GTPases Rac1, Cdc42 and RhoA in a signaling axis triggered by its phosphorylation and interaction with Cbl phosphorylated on tyrosine 774. We also gained insights on the functional transport of CD93 during adhesion and migration, demonstrating that it is regulated by both its cytoplasmic domain and the Rab5C-
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Seo, Wooseok. "Functional analysis of murine CD43 shedding : a role for the CD43 cytoplasmic tail in nuclear signalling." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/629.

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CD43, a representative of the leukocyte mucin family proteins, is a transmembrane protein highly expressed on most lymphohemopoietic cells and is believed to play a role in the regulation of leukocyte activation and/or migration. CD43 was shown to be proteolytically shed from human cells and high concentrations of soluble CD43 have been found in human plasma. The biological significance of CD43 shedding however remains enigmatic. To study the functional significance of CD43 shedding, we initiated our study by investigating whether CD43 shedding also occurs in the murine system and confirmed using flow cytometry, Western blot and ELISA techniques that murine CD43 is cleaved from the cell surface as is observed in the human system. To examine the biological significance of CD43 shedding, we designed and constructed non-sheddable forms of murine CD43. Ectopic expression of non-sheddable CD43 molecules in primary CD43 deficient bone marrow cells showed that these CD43 mutants have serious negative impacts on cell viability, revealing CD43 shedding as an essential process and implying that the CD43 mutants interfered with intracellular signaling processes. Our data support the hypothesis that CD43 ectodomain shedding is a requirement for release of the cytoplasmic domain and its translocation to the nucleus. In support of our hypothesis, we confirmed that the CD43 cytoplasmic domain is localized in the nucleus and is modified by SUMO (small ubiquitin-like modifier) peptides. In an attempt to determine the functional significance of CD43 nuclear translocation and SUMO modification, we examined nuclei from hemopoietic cells more closely and observed that the CD43 cytoplasmic tail is localized in a subnuclear structure called promyelocytic nuclear bodies, which control many nuclear functions including apoptosis. Consistent with this observation we find that leukocytes from CD43 deficient mice have an increased apoptotic response upon growth factor withdrawal. We conclude that nuclear translocation of the CD43 cytoplasmic tail serves to control the apoptotic response in leukocytes and that CD43 functions as an anti-apoptotic molecule.
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Greaves, Sarah Jennifer. "Analysis of cd9b in CXCR4b signalling." Thesis, University of Sheffield, 2016. http://etheses.whiterose.ac.uk/13921/.

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CXCR4b, CXCR7b and their ligand, CXCL12a, are essential for the migration of the posterior lateral line primordium (pLLP) and primordial germ cells (PGCs) in zebrafish (Dambly-Chaudière et al. 2007, Boldajipour et al. 2008). A number of tetraspanins have been shown to affect CXCR4-mediated processes through regulating CXCR4 trafficking or downstream signalling (Yoshida et al. 2008, Li et al. 2011, Leung et al. 2011). Based upon these results we set out to identify candidate tetraspanins that may play a similar role in CXCR4b signalling during pLLP and PGC migration. CD9b, one of the zebrafish homologs of human CD9, was identified as a good candidate gene. Morpholino knock down of cd9b, using either a translation-blocking or splice-site blocking morpholino, resulted in reduced neuromast deposition and abnormal structure of the posterior lateral line. However, morpholinos often have nonspecific effects and so two CD9b knockout lines were created using TALENs. Surprisingly CD9b homozygous mutants showed normal lateral line structure. Preliminary results suggest that the phenotype differences between CD9b morphants and mutants may be due to residual functionality in the wildtype N-terminal of CD9b, upstream of the mutation site, in CD9b mutants. As well as assessment of PGC and pLLP migration, CD9b mutants were also assessed for fertility defects. Significantly reduced numbers of pups are born to CD9 knockout mice. This is due to a requirement of CD9 on the egg membrane for efficient sperm-egg fusion in the CD9-/- female mice (Kaji et al. 2000, Le Naour et al. 2000, Miyado et al. 2000). CD9b -/- zebrafish also appear to have fertility defects. Fewer eggs were laid by CD9b -/- zebrafish pairs and of the eggs laid, a lower percentage were fertilised.
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Brosig, Susann. "Signaltransduktion von CD97 in humanen Fibrosarkomzellen." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-164004.

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CD97 gehört zur Familie der Adhäsions-G-Protein gekoppelten Rezeptoren (aGPCR), die aus einem langen extrazellulären N-terminalen Fragment (NTF) und einem nicht-kovalent gekoppelten C-terminalen Fragment (CTF) mit der sieben-transmembranären (TM7) Region und dem intrazellulären Teil bestehen. CD97 wird in malignen Tumoren exprimiert. In der humanen Fibrosarkomzelllinie HT1080 steigert die stabile Überexpression von CD97 die ungerichtete zweidimensionale (2D) Migration einzelner Zellen. Eine Verkürzung von CD97 im CTF auf zwei transmembranäre (TM2) Domänen führt zu einer Suppression der 2D-Migration im Vergleich zu stabil mock-transfektierten HT1080 Kontrollzellen. Wahrscheinlich supprimiert CD97/TM2 die endogene CD97-Wirkung. Unbekannt ist, welche Signalwege durch CD97-Überexpression in HT1080 reguliert werden und welche Signalwege für die Migrationssteigerung von HT1080 verantwortlich sind. Die Klärung dieser Signalwege ist Gegenstand der vorliegenden Arbeit. Die Phosphorylierung von Proteinkinasen ist eine posttranslationale Modifikation zur Regulation der Kinaseaktivität mit nachfolgender Aktivierung oder Inaktivierung eines Signalweges. Daher sind Expression und Phosphorylierung der Proteinkinasen zur Identifikation regulierter Signalwege interessant. Dazu wurden in Lysaten von CD97/TM7, CD97/TM2 und mock-transfektierten HT1080 mittels Kinetworks Phosphosite Screen KPSS 1.3 Profiling (Multi-Immunoblot™) 37 verschiedene Proteinphosphorylierungen untersucht und regulierte Signalwege identifiziert. An 25 Phosphorylierungsstellen erfolgt eine Regulation durch CD97. Anschließend wurden die Ergebnisse der interessantesten Proteine hinsichtlich ihrer Expression und Phosphorylierung im Western Blot verifiziert und um Proteine erweitert, die klassisch an der Regulation der Zellmigration beteiligt sind. Es zeigt sich eine Aktivierung des PI3-Kinase/Akt-Signalweges und eine Inhibierung von Src durch CD97. 2D-Migrationsversuche von HT1080 CD97/TM7, CD97/TM2 und mock mit spezifischen Inhibitoren gegen den PI3-Kinase/Akt-Signalweg und gegen Src bestätigen, dass diese Kinasen an der CD97-induzierten Steigerung der 2D-Migration beteiligt sind. Weiterhin finden sich Hinweise, dass in HT1080 CD97 die Apoptose hemmt und die Proliferation reguliert. Insgesamt wird in dieser Arbeit ein Überblick über die durch CD97 regulierten Signalwege gegeben. Die CD97-gesteigerte 2D-Migration von HT1080 wird durch eine Aktivierung des PI3-Kinase/ Akt-Signalweges und Inhibierung von Src vermittelt.
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Thomas, Mélissa. "Etude de la voie non-apoptotique de CD95 et de l’implication du facteur d’initiation de la traduction eIF4A1." Thesis, Rennes 1, 2018. http://www.theses.fr/2018REN1B048.

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Depuis sa découverte en 1991, l’implication du récepteur CD95 dans l’induction de l’apoptose a été plus que largement décrite. Mais bien qu'ayant été identifié comme étant un récepteur de mort, CD95 est aussi capable d'induire un signal pro-oncogénique lorsqu'il est fixé au CD95L clivé. L’activation de cette voie de signalisation non-apoptotique par le s-CD95L contribue au processus inflammatoire dans le lupus et à la dissémination métastatique dans les cancers du sein triples négatifs. Cependant aucun traitement thérapeutique satisfaisant n’est à ce jour disponible. De par son implication dans des pathologies cancéreuses et inflammatoires, mieux comprendre les mécanismes à l’origine de la double signalisation de CD95 n’est plus un enjeu mais une nécessité. Afin de développer des molécules pour bloquer la signalisation non apoptotique de CD95, il est essentiel d’en identifier tous les protagonistes et de définir leur fonction biologique. C’est avec cet objectif que notre équipe a mené deux études protéomiques dont les résultats ont permis d’identifier eIF4A1 comme un nouveau partenaire direct de CD95. Nous montrons que eIF4A1 est indispensable à la mise en place de la signalisation pro-motile de CD95 dépendante de la voie PI3K. De plus eIF4A1 est recruté à la membrane ainsi que les autres protéines du complexe eIF4F. Nos données de séquençage ont montré que de par cette interaction, CD95 recrute à la membrane un ensemble d’ARNm impliqués dans la réponse immunitaire et l’adhésion cellulaire. En outre, une perte de CD95 dans certaines cellules cancéreuses conduit à la perte d’expression de ces ARNm. Ainsi CD95 pourrait protéger certains ARNm de la dégradation et favoriser la traduction des ARNm pro-inflammatoires de manière indépendante du ligand. Cibler spécifiquement cette interaction pourrait être une piste thérapeutique prometteuse dans la lutte contre les cancers du sein triples négatifs mais aussi contre le lupus
Since its discovery in 1991, the involvement of the CD95 receptor in the induction of apoptosis has been more than widely described. But although identified as a death receptor, CD95 is also capable of inducing a pro-oncogenic signal when attached to the cleaved CD95L. Activation of this non-apoptotic signaling pathway by s-CD95L contributes to the inflammatory process in lupus and metastatic spread in triple negative breast cancers. However, no satisfactory therapeutic treatment is currently available. By its implication in cancerous and inflammatory pathologies, better understanding the mechanisms at the origin of the double signaling of CD95 is no longer an issue but a necessity. In order to develop molecules to block the non-apoptotic CD95 signaling, it is essential to identify all the protagonists and define their biological function. Our team conducted two proteomic studies, the results of which identified eIF4A1 as a new direct partner of CD95. We show that eIF4A1 is essential for the implementation of PI3K pathway-dependent CD95 signaling. In addition eIF4A1 is recruited to the membrane as well as the other eIF4F complex proteins. Our sequencing data showed that by this interaction, CD95 recruits a set of mRNAs involved in the immune response and cell adhesion. In addition, a loss of CD95 in some cancer cells leads to the loss of expression of these mRNAs. Thus CD95 could protect certain mRNA from degradation and promote the translation of pro-inflammatory mRNAs independently of the ligand. Specific targeting of this interaction could be a promising therapeutic avenue in the fight against triple negative breast cancers but also against lupus
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Georgieva, Petya [Verfasser]. "Microglial purinergic signaling in mouse models of CD39 deficiency and schizophrenia / Petya Georgieva." Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1069290173/34.

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Yamaoka, Ryoya. "CD90 expression in human intrahepatic cholangiocarcinoma is associated with lymph node metastasis and poor prognosis." Kyoto University, 2019. http://hdl.handle.net/2433/242375.

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Doma, Eszter. "Identification of noval critical steps in the early and late Fas signaling pathway : the role of Fas tyrosine phosphorylation and the formation of Fas complexes." Nice, 2009. http://www.theses.fr/2009NICE4078.

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Fas est un récepteur de mort de la superfamille des récepteurs au TNF (TNFR). Il est exprimé constitutivement dans de nombreux tissus et joue un rôle important dans l’homéostasie lymphocytaire. Suite à la liaison de son ligand (FasL), il est rapidement internalisé puis recrute les protéines FADD et procaspase-8 pour former le DISC (death-inducing signaling complex), conduisant ainsi à l��activation des caspases et la mort de la cellule. De nombreux travaux suggèrent que Fas, en plus d’être un récepteur de mort, peut transmettre des fonctions alternatives ou de survie. Or, le mécanisme moléculaire contrôlant l’orientation de la signalisation vers ces fonctions n’est pas élucidé. Cette thèse est focalisée sur deux aspects différents de la signalisation par Fas afin de préciser ses mécanismes de régulation. Deux tyrosines intracellulaires de Fas sont localisées dans des motifs importants pour la phosphorylation et l’internalisation. Nous avons démontré que ces deux résidus ont un rôle critique dans la mort induite par Fas. Cependant, ils ont profil de phosphorylation différent et recrutent différents adaptateurs ? Ainsi, comme d’autres importants régulateurs de la signalisation de Fas, son profil de phosphorylation pourrait représenter un des événements précoces responsable de la bifurcation du signal vers des voies de mort ou de survie. Pendant la phase d’exécution de la mort par Fas, nous avons observé la formation de différents complexes de Fas stables en présence de SDS. Ceci a lieu en aval du DISC et nécessite l’activité des caspases. Ces complexes diffèrent entre eux quant à la nécessité d’un cytosquelette d’actine et microtubulaire intègre pour leur formation. Ainsi, nous avons identifié un nouveau rôle des microtubules dans l’organisation des molécules de Fas pendant l’apoptose. L’ensemble de ces résultats a é=révélé certaines nouvelles étapes dans les phases très précoces et tardives de la signalisation par Fas et qui contribuent à la compréhension de la versatilité fonctionnelle de Fas
Fas is a prototypic death receptor of the tumor necrosis factor receptor (TNFR) superfamily. It is constitutively expressed in a wide range of tissues and plays a particularly important role in the lymphocyte homeostasis. Upon engagement by its ligand (FastL), it undergoes rapid internalization, whereupon the adapter FADD and the caspase-8 proenzyme are recruited to form the death-inducing signalling complex (DISC), leading to caspase activation and cell death. Accumulating evidence suggests that Fas, besides being a death-inducing receptor, can also mediate a variety of non-death activities. However the precise molecular mechanism of the divergence of these two pathways is not fully understood. This thesis is focused on two different aspects of the Fas signalling in order to gain deeper in sight in its precise regulation. We found that the intracellular tyrosines of Fas are located in important phosphorylation and internalization sorting motives, and therefore focused on the role of the receptor tyrosine phosphorylation. We show that the two tyrosine residues are critical for Fas mediated cell death. However they have different phosphorylation pattern and adaptor recruitments. As important regulators of internalization and downstream signalling, Fas tyrosine phosphorylation pattern might be one of the early events which are responsible for the bifurcation of the cell death and survival pathways. At the execution phase of FasL-induced apoptosis we noticed the formation of distinct SDS-stable Fas complexes. This complex formation occurs downstream of the DISC assembly and requires distinct caspase activities. Subgroup of Fas complexes differ in the requirement for the integrity of actin and microtubular cytoskeleton. Consequently, we identified a novel role of microtubule in the organization of Fas molecules during apoptosis. Altogether, the findings reveal some new steps in the very early and late stages of Fas signalling which contribute to the understanding of its functional versatility
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Pawar, Pritish Subhash. "Calmodulin binding to cellular FLICE like inhibitory protein modulates Fas-induced signaling and tumorigenesis in cholangiocarcinoma." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008p/pawar.pdf.

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Chen, Si [Verfasser], and Ana [Akademischer Betreuer] Martin-Villalba. "The CD95/CD95L signaling system in developmental and tumor angiogenesis of the central nervous system / Si Chen ; Betreuer: Ana Martin-Villalba." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177688484/34.

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Books on the topic "CD93 signaling"

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Fas Signaling. Springer, 2006.

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Book chapters on the topic "CD93 signaling"

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Kinner-Bibeau, Laurén B., Sudesh Pawaria, and Robert J. Binder. "CD91." In Encyclopedia of Signaling Molecules, 968–74. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_413.

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Torres-Huerta, Alvaro, Estefania Aleman-Navarro, Maria Elena Bravo-Adame, Monserrat Alba Sandoval-Hernandez, Oscar Arturo Migueles-Lozano, and Yvonne Rosenstein. "CD43." In Encyclopedia of Signaling Molecules, 893–905. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_523.

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Lazo, Pedro A., Mónica Yunta, and Ramiro Barcia. "CD53." In Encyclopedia of Signaling Molecules, 930–37. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_566.

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Kinner-Bibeau, Laurén B., Sudesh Pawaria, and Robert J. Binder. "CD91." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_413-1.

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Torres-Huerta, Alvaro, Estefania Aleman-Navarro, Maria Elena Bravo-Adame, Monserrat Alba Sandoval-Hernandez, Oscar Arturo Migueles-Lozano, and Yvonne Rosenstein. "CD43." In Encyclopedia of Signaling Molecules, 1–13. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_523-1.

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Lazo, Pedro A., Mónica Yunta, and Ramiro Barcia. "CD53." In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_566-1.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CD39." In Encyclopedia of Signaling Molecules, 306. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100201.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CD91." In Encyclopedia of Signaling Molecules, 359–64. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_413.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CD43." In Encyclopedia of Signaling Molecules, 320–28. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_523.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CD53." In Encyclopedia of Signaling Molecules, 343–47. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_566.

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Conference papers on the topic "CD93 signaling"

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Schindler, Ulrike, Joanne B. Tan, Matt Walters, Annette Becker, Fangfang Yin, Ada Chen, Yu Chen, et al. "Abstract 2640: Small-molecule inhibitors of CD73, CD39 and A2aR: Three anti-cancer targets in the ATP/adenosine signaling pathway." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2640.

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"Computational design of molecular probes targeting CD95 signaling pathway." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-581.

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Gieffers, Christian, Harald Fricke, Wick Wolfgang, and Ana Martin-Villalba. "Abstract LB-273: Inhibition of CD95-dependent signaling for the treatment of glioblastoma multiforme." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-273.

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Brzoska, T., E. V. Menchikova, T. W. Kaminski, R. Vats, E. Tutuncuoglu, S. P. Tofovic, E. K. Jackson, M. T. Gladwin, and P. Sundd. "CD39-Bearing Extracellular Vesicles Constrain Platelet Purinergic Signaling-Dependent Pulmonary Thrombosis in Sickle Cell Disease." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5190.

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Chiu, Huan-Chih, Chin-Ting Huang, Teng-Yuan Chang, and John T. A. Hsu. "Abstract B211: Augmentation of Fas (CD95) signaling pathway sensitizes non-small cell lung cancer (NSCLC) cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b211.

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Leshkova, I. V., O. V. Dolgih, and O. YU Ustinova. "IMMUNOLOGICAL DISORDERS OF THE REPRODUCTIVE SYSTEM THAT OCCUR WHEN EXPOSED TO BENZENE, IN EMPLOYEES OF OIL-PRODUCING ENTERPRISES." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-313-316.

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Abstract. Introduction. The protection of the reproductive health of the working-age population is the most important direction of State policy. In 5-15% of cases, the causes of reproductive dysfunction are immunological disorders. Benzene belongs to the group of industrial reprotoxicants, however, its effect of benzene on the reproductive system has not been sufficiently studied. Objective: to study the immunological aspects of the effect of benzene on the reproductive system. Methods. We examined 50 men exposed to benzene with reproductive disorders (26-49 years old), as well as 4 workers with normal sexual function aged 53-60 years. Spontaneous and induced changes in the cellular expression of apoptosis markers were studied. For the study, the ANNEXIN V-FITC/7-AAD kit was used for the detection of cells that have undergone apoptosis. The experiment was conducted in vitro using a biological medium (ejaculate). A factor of the chemical nature was benzene. Results. According to the results of the comparative analysis, there were no significant deviations of pathogenetic tests of immunological markers in comparison with the reference level in the spontaneous expression samples, but there was an excess of expression of the CD95 + cell death receptor (p<0.05) in 30% of the samples examined, and a decrease in the number of Annexin V-FITC+7AAD negative cells (without reaching the significance level) in samples with a load of (15%). There was a difference in the expression levels of CD95+ and CD25+ CD-reception indicators by 20% and 10% in relation to the spontaneous level (p<0.05). Representatives of the chemical group of aromatic hydrocarbons realize reprotoxicity, using the mechanism of excessive induction of the membrane signaling of the cell death receptor, accelerate the natural program of cell death by approximately 20% compared to the state of reproductive cells that were not stimulated. Conclusion. At the present stage, one of the tasks of occupational medicine is to study the effect of chemicals on the processes of reproduction, to develop new approaches to assessing the risk of their impact on the reproductive health of workers.
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Katsuta, Eriko, Vivek Anand, Li Yan, Subhamoy Dasgupta, and Kazuaki Takabe. "Abstract 5200: High CD73 expression, regulated by estrogen signaling, associates with cancer aggressiveness in estrogen receptor (+) breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5200.

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Katsuta, Eriko, Vivek Anand, Li Yan, Subhamoy Dasgupta, and Kazuaki Takabe. "Abstract 5200: High CD73 expression, regulated by estrogen signaling, associates with cancer aggressiveness in estrogen receptor (+) breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5200.

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Huang, Jian, Alexander Craig Mackinnon, and Liying Jiang. "Abstract 1210: Tetraspanin CD63 interacts with extranuclear estrogen receptor alpha and regulates non-genomic signaling pathways in breast cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1210.

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Ventura, Selena, Chiara Manzalini, Dave Aryee, Piero Picci, Heinrich Kovar, and Katia Scotlandi. "Abstract 481: Dualistic regulation of NF-kB signaling by CD99 and EWS-FLI1 in Ewing sarcoma: impact on cell differentiation." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-481.

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