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10.4049/jimmunol.1401798 http://scihub22266oqcxt.onion/10.4049/jimmunol.1401798 C4259264!4259264 !25362179     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25362179 &cmd=llinks): Failed to open stream: HTTP request failed! 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DBC1 is a suppressor of B cell activation by negatively regulating alternative NF-?B transcriptional activity |pdf=|usr=}}{{25362179 }} gab.com Text DBC1 is a suppressor of B cell activation by negatively regulating alternative NF- B transcriptional activity JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25362179 #FOAvip CD40 and BAFFR signaling play important roles in B cell proliferation and Ig production. In this study, we found that B cells from mice with deletion of Dbc1 gene (Dbc1(-/-)) show elevated proliferation, and IgG1 and IgA production upon in vitro CD40 and BAFF, but not BCR and LPS stimulation, indicating that DBC1 inhibits CD40/BAFF-mediated B cell activation in a cell-intrinsic manner. Microarray analysis and chromatin immunoprecipitation experiments reveal that DBC1 inhibits B cell function by selectively suppressing the transcriptional activity of alternative NF-?B members RelB and p52 upon CD40 stimulation. As a result, when immunized with nitrophenylated-keyhole limpet hemocyanin, Dbc1(-/-) mice produce significantly increased levels of germinal center B cells, plasma cells, and Ag-specific Ig. Finally, loss of DBC1 in mice leads to higher susceptibility to experimental autoimmune myasthenia gravis. Our study identifies DBC1 as a novel regulator of B cell activation by suppressing the alternative NF-?B pathway. Twit Text FOAVip DBC1 is a suppressor of B cell activation by negatively regulating alternative NF- B transcriptional activity ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25362179 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25362179 #FOAvip English Wikipedia <ref>{{Cite pmid|25362179 }}</ref> DBC1 is a suppressor of B cell activation by negatively regulating alternative NF-?B transcriptional activity #MMPMID25362179 Kong S ; Thiruppathi M ; Qiu Q ; Lin Z ; Dong H ; Chini EN ; Prabhakar BS ; Fang D J Immunol 2014[Dec]; 193 (11 ): 5515-24 PMID25362179 show ga CD40 and BAFFR signaling play important roles in B cell proliferation and Ig production. In this study, we found that B cells from mice with deletion of Dbc1 gene (Dbc1(-/-)) show elevated proliferation, and IgG1 and IgA production upon in vitro CD40 and BAFF, but not BCR and LPS stimulation, indicating that DBC1 inhibits CD40/BAFF-mediated B cell activation in a cell-intrinsic manner. Microarray analysis and chromatin immunoprecipitation experiments reveal that DBC1 inhibits B cell function by selectively suppressing the transcriptional activity of alternative NF-?B members RelB and p52 upon CD40 stimulation. As a result, when immunized with nitrophenylated-keyhole limpet hemocyanin, Dbc1(-/-) mice produce significantly increased levels of germinal center B cells, plasma cells, and Ag-specific Ig. Finally, loss of DBC1 in mice leads to higher susceptibility to experimental autoimmune myasthenia gravis. Our study identifies DBC1 as a novel regulator of B cell activation by suppressing the alternative NF-?B pathway. |Animals [MESH] |Antibody Formation/genetics [MESH] |B-Cell Activating Factor/metabolism [MESH] |B-Lymphocytes/*immunology [MESH] |CD40 Antigens/metabolism [MESH] |Cell Cycle Proteins [MESH] |Cell Differentiation/genetics [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Immune Tolerance [MESH] |Lymphocyte Activation/genetics [MESH] |Mice [MESH] |Mice, Inbred Strains [MESH] |Mice, Knockout [MESH] |Microarray Analysis [MESH] |Myasthenia Gravis, Autoimmune, Experimental/genetics/*immunology [MESH] |NF-kappa B/genetics/*metabolism [MESH] |NIH 3T3 Cells [MESH] |Nerve Tissue Proteins/genetics/*metabolism [MESH] |Plasma Cells/*immunology [MESH]DBC1 is a suppressor of B cell activation by negatively regulating alt(epmc).pdf DeepDyve Pubget Overpricing