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10.1038/s41467-017-01475-7 http://scihub22266oqcxt.onion/10.1038/s41467-017-01475-7 C5682283!5682283 !29129929     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29129929 &cmd=llinks): Failed to open stream: HTTP request failed! 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IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression |pdf=|usr=}}{{29129929 }} gab.com Text IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29129929 #FOAvip Plasma cell differentiation is a tightly regulated process that requires appropriate T cell helps to reach the induction threshold. To further understand mechanisms by which T cell inputs regulate B cell fate decision, we investigate the minimal IL-2 stimulation for triggering human plasma cell differentiation in vitro. Here we show that the timed repression of BACH2 through IL-2-mediated ERK/ELK1 signalling pathway directs plasma cell lineage commitment. Enforced BACH2 repression in activated B cells unlocks the plasma cell transcriptional program and induces their differentiation into immunoglobulin M-secreting cells. RNA-seq and ChIP-seq results further identify BACH2 target genes involved in this process. An active regulatory region within the BACH2 super-enhancer, under ELK1 control and differentially regulated upon B-cell activation and cellular divisions, helps integrate IL-2 signal. Our study thus provides insights into the temporal regulation of BACH2 and its targets for controlling the differentiation of human naive B cells. Twit Text FOAVip IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29129929 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29129929 #FOAvip English Wikipedia <ref>{{Cite pmid|29129929 }}</ref> IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression #MMPMID29129929 Hipp N ; Symington H ; Pastoret C ; Caron G ; Monvoisin C ; Tarte K ; Fest T ; Delaloy C Nat Commun 2017[Nov]; 8 (1 ): 1443 PMID29129929 show ga Plasma cell differentiation is a tightly regulated process that requires appropriate T cell helps to reach the induction threshold. To further understand mechanisms by which T cell inputs regulate B cell fate decision, we investigate the minimal IL-2 stimulation for triggering human plasma cell differentiation in vitro. Here we show that the timed repression of BACH2 through IL-2-mediated ERK/ELK1 signalling pathway directs plasma cell lineage commitment. Enforced BACH2 repression in activated B cells unlocks the plasma cell transcriptional program and induces their differentiation into immunoglobulin M-secreting cells. RNA-seq and ChIP-seq results further identify BACH2 target genes involved in this process. An active regulatory region within the BACH2 super-enhancer, under ELK1 control and differentially regulated upon B-cell activation and cellular divisions, helps integrate IL-2 signal. Our study thus provides insights into the temporal regulation of BACH2 and its targets for controlling the differentiation of human naive B cells. |Basic-Leucine Zipper Transcription Factors/*antagonists & inhibitors/genetics [MESH] |Cell Differentiation/*immunology [MESH] |Cells, Cultured [MESH] |Extracellular Signal-Regulated MAP Kinases/*metabolism [MESH] |Gene Regulatory Networks/immunology [MESH] |Humans [MESH] |Immunoglobulin M/biosynthesis/immunology [MESH] |Interleukin-2/*immunology [MESH] |Lymphocyte Activation/immunology [MESH] |Plasma Cells/*cytology/immunology [MESH] |Positive Regulatory Domain I-Binding Factor 1/biosynthesis [MESH] |RNA Interference [MESH] |RNA, Small Interfering/genetics [MESH] |Signal Transduction/immunology [MESH] |T-Lymphocytes/immunology [MESH] |X-Box Binding Protein 1/biosynthesis [MESH]IL-2 imprints human naive B cell fate towards plasma cell through ER(epmc).pdf DeepDyve Pubget Overpricing