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10.1038/jid.2014.519 http://scihub22266oqcxt.onion/10.1038/jid.2014.519 C4366298!4366298 !25501661     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25501661 &cmd=llinks): Failed to open stream: HTTP request failed! 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RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppression of NF-?B-dependent inflammation |pdf=|usr=}}{{25501661 }} gab.com Text RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppression of NF- B-dependent inflammation JO: J Invest Dermatol http://www.kidney.de/pget.php?&tw=1&pmid=25501661 #FOAvip Mice with epidermal deletion of JunB transcription factor displayed a psoriasis-like inflammation. The relevance of these findings to humans and the mechanisms mediating JunB function are not fully understood. Here we demonstrate that impaired JunB function via gene silencing or overexpression of a dominant negative mutant increased human keratinocyte cell proliferation but decreased cell barrier function. RNA-seq revealed over 500 genes affected by JunB loss of function, which included the upregulation of an array of proinflammatory molecules relevant to psoriasis. Among these were tumor necrosis factor ? (TNF?), CCL2, CXCL10, IL6R, and SQSTM1, an adaptor protein involved in nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B) activation. Chromatin immunoprecipitation (ChIP)-Seq and gene reporter analyses showed that JunB directly suppressed SQSTM1 by binding to a consensus AP-1 cis element located around 2?kb upstream of SQSTM1-transcription start site. Similar to JunB loss of function, SQSTM1-overexpression induced TNF?, CCL2, and CXCL10. Conversely, NF-?B inhibition genetically with a mutant I?B? or pharmacologically with pyrrolidine dithiocarbamate (PDTC) prevented cytokine, but not IL6R, induction by JunB deficiency. Taken together, our findings indicate that JunB controls epidermal growth, barrier formation, and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB suppression of NF-?B-dependent inflammation. Twit Text FOAVip RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppression of NF- B-dependent inflammation ????J Invest Dermatol http://www.kidney.de/pget.php?&tw=1&pmid=25501661 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25501661 #FOAvip English Wikipedia <ref>{{Cite pmid|25501661 }}</ref> RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppression of NF-?B-dependent inflammation #MMPMID25501661 Zhang X ; Jin JY ; Wu J ; Qin X ; Streilein R ; Hall RP ; Zhang JY J Invest Dermatol 2015[Apr]; 135 (4 ): 1016-1024 PMID25501661 show ga Mice with epidermal deletion of JunB transcription factor displayed a psoriasis-like inflammation. The relevance of these findings to humans and the mechanisms mediating JunB function are not fully understood. Here we demonstrate that impaired JunB function via gene silencing or overexpression of a dominant negative mutant increased human keratinocyte cell proliferation but decreased cell barrier function. RNA-seq revealed over 500 genes affected by JunB loss of function, which included the upregulation of an array of proinflammatory molecules relevant to psoriasis. Among these were tumor necrosis factor ? (TNF?), CCL2, CXCL10, IL6R, and SQSTM1, an adaptor protein involved in nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B) activation. Chromatin immunoprecipitation (ChIP)-Seq and gene reporter analyses showed that JunB directly suppressed SQSTM1 by binding to a consensus AP-1 cis element located around 2?kb upstream of SQSTM1-transcription start site. Similar to JunB loss of function, SQSTM1-overexpression induced TNF?, CCL2, and CXCL10. Conversely, NF-?B inhibition genetically with a mutant I?B? or pharmacologically with pyrrolidine dithiocarbamate (PDTC) prevented cytokine, but not IL6R, induction by JunB deficiency. Taken together, our findings indicate that JunB controls epidermal growth, barrier formation, and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB suppression of NF-?B-dependent inflammation. |Adaptor Proteins, Signal Transducing/*genetics/metabolism [MESH] |Animals [MESH] |Cell Adhesion [MESH] |Cell Proliferation [MESH] |Chemokine CCL2/metabolism [MESH] |Chemokine CXCL10/metabolism [MESH] |Chromatin Immunoprecipitation [MESH] |Cytokines/metabolism [MESH] |Epidermis/metabolism [MESH] |Gene Deletion [MESH] |Genes, Reporter [MESH] |HEK293 Cells [MESH] |Heat-Shock Proteins/*genetics/metabolism [MESH] |Humans [MESH] |Inflammation/*metabolism [MESH] |Keratinocytes/cytology [MESH] |Mice [MESH] |Mutation [MESH] |NF-kappa B/*metabolism [MESH] |Oligonucleotide Array Sequence Analysis [MESH] |Pyrrolidines/chemistry [MESH] |Regeneration [MESH] |Sequence Analysis, RNA [MESH] |Sequestosome-1 Protein [MESH] |Skin Physiological Phenomena [MESH] |Thiocarbamates/chemistry [MESH]RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppr(epmc).pdf DeepDyve Pubget Overpricing