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10.1101/gad.267245.115 http://scihub22266oqcxt.onion/10.1101/gad.267245.115 C4604346!4604346 !26443849     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26443849 &cmd=llinks): Failed to open stream: HTTP request failed! 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Widespread JNK-dependent alternative splicing induces a positive feedback loop through CELF2-mediated regulation of MKK7 during T-cell activation |pdf=|usr=}}{{26443849 }} gab.com Text Widespread JNK-dependent alternative splicing induces a positive feedback loop through CELF2-mediated regulation of MKK7 during T-cell activation JO: Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=26443849 #FOAvip Alternative splicing is prevalent among genes encoding signaling molecules; however, the functional consequence of differential isoform expression remains largely unknown. Here we demonstrate that, in response to T-cell activation, the Jun kinase (JNK) kinase MAP kinase kinase 7 (MKK7) is alternatively spliced to favor an isoform that lacks exon 2. This isoform restores a JNK-docking site within MKK7 that is disrupted in the larger isoform. Consistently, we show that skipping of MKK7 exon 2 enhances JNK pathway activity, as indicated by c-Jun phosphorylation and up-regulation of TNF-?. Moreover, this splicing event is itself dependent on JNK signaling. Thus, MKK7 alternative splicing represents a positive feedback loop through which JNK promotes its own signaling. We further show that repression of MKK7 exon 2 is dependent on the presence of flanking sequences and the JNK-induced expression of the RNA-binding protein CELF2, which binds to these regulatory elements. Finally, we found that ?25% of T-cell receptor-mediated alternative splicing events are dependent on JNK signaling. Strikingly, these JNK-dependent events are also significantly enriched for responsiveness to CELF2. Together, our data demonstrate a widespread role for the JNK-CELF2 axis in controlling splicing during T-cell activation, including a specific role in propagating JNK signaling. Twit Text FOAVip Widespread JNK-dependent alternative splicing induces a positive feedback loop through CELF2-mediated regulation of MKK7 during T-cell activation ????Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=26443849 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26443849 #FOAvip English Wikipedia <ref>{{Cite pmid|26443849 }}</ref> Widespread JNK-dependent alternative splicing induces a positive feedback loop through CELF2-mediated regulation of MKK7 during T-cell activation #MMPMID26443849 Martinez NM ; Agosto L ; Qiu J ; Mallory MJ ; Gazzara MR ; Barash Y ; Fu XD ; Lynch KW Genes Dev 2015[Oct]; 29 (19 ): 2054-66 PMID26443849 show ga Alternative splicing is prevalent among genes encoding signaling molecules; however, the functional consequence of differential isoform expression remains largely unknown. Here we demonstrate that, in response to T-cell activation, the Jun kinase (JNK) kinase MAP kinase kinase 7 (MKK7) is alternatively spliced to favor an isoform that lacks exon 2. This isoform restores a JNK-docking site within MKK7 that is disrupted in the larger isoform. Consistently, we show that skipping of MKK7 exon 2 enhances JNK pathway activity, as indicated by c-Jun phosphorylation and up-regulation of TNF-?. Moreover, this splicing event is itself dependent on JNK signaling. Thus, MKK7 alternative splicing represents a positive feedback loop through which JNK promotes its own signaling. We further show that repression of MKK7 exon 2 is dependent on the presence of flanking sequences and the JNK-induced expression of the RNA-binding protein CELF2, which binds to these regulatory elements. Finally, we found that ?25% of T-cell receptor-mediated alternative splicing events are dependent on JNK signaling. Strikingly, these JNK-dependent events are also significantly enriched for responsiveness to CELF2. Together, our data demonstrate a widespread role for the JNK-CELF2 axis in controlling splicing during T-cell activation, including a specific role in propagating JNK signaling. |*Gene Expression Regulation [MESH] |Alternative Splicing/*genetics [MESH] |CD4-Positive T-Lymphocytes/cytology/metabolism [MESH] |CELF Proteins/*metabolism [MESH] |Feedback, Physiological/physiology [MESH] |Humans [MESH] |JNK Mitogen-Activated Protein Kinases/*genetics/*metabolism [MESH] |Jurkat Cells [MESH] |MAP Kinase Kinase 7/*genetics/metabolism [MESH] |Nerve Tissue Proteins/*metabolism [MESH] |RNA Stability/genetics [MESH] |Signal Transduction/genetics [MESH]Widespread JNK-dependent alternative splicing induces a positive feedb(epmc).pdf DeepDyve Pubget Overpricing