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10.4049/jimmunol.1700023 http://scihub22266oqcxt.onion/10.4049/jimmunol.1700023 C5531076!5531076 !28626066     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28626066 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cytoplasmic Form of Carlr lncRNA Facilitates Inflammatory Gene Expression upon NF-?B Activation |pdf=|usr=}}{{28626066 }} gab.com Text Cytoplasmic Form of Carlr lncRNA Facilitates Inflammatory Gene Expression upon NF- B Activation JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28626066 #FOAvip Long noncoding RNAs (lncRNAs) have emerged as critical regulators of inflammation. To further understand the interaction between inflammatory signaling pathways and lncRNAs, we characterized the function of cardiac and apoptosis-related lncRNA (Carlr), an lncRNA expressed in both mouse and human cells of diverse tissues. Carlr expression is increased following NF-?B signaling in macrophages, with concomitant translocation to, and enrichment of, the transcript in the cytoplasm. Knockdown of Carlr results in impaired expression of NF-?B pathway genes and influences the interaction between macrophages and intestinal cells in an inflammatory environment. In human celiac disease patient samples, increased levels of the Carlr transcript were detected in the cytoplasm, alongside elevated expression of NF-?B pathway genes. These findings suggest that increased Carlr expression and/or cytoplasmic localization is required for efficient NF-?B signaling and is associated with the inflamed tissue state observed in human celiac disease. Twit Text FOAVip Cytoplasmic Form of Carlr lncRNA Facilitates Inflammatory Gene Expression upon NF- B Activation ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28626066 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28626066 #FOAvip English Wikipedia <ref>{{Cite pmid|28626066 }}</ref> Cytoplasmic Form of Carlr lncRNA Facilitates Inflammatory Gene Expression upon NF-?B Activation #MMPMID28626066 Castellanos-Rubio A ; Kratchmarov R ; Sebastian M ; Garcia-Etxebarria K ; Garcia L ; Irastorza I ; Ghosh S J Immunol 2017[Jul]; 199 (2 ): 581-588 PMID28626066 show ga Long noncoding RNAs (lncRNAs) have emerged as critical regulators of inflammation. To further understand the interaction between inflammatory signaling pathways and lncRNAs, we characterized the function of cardiac and apoptosis-related lncRNA (Carlr), an lncRNA expressed in both mouse and human cells of diverse tissues. Carlr expression is increased following NF-?B signaling in macrophages, with concomitant translocation to, and enrichment of, the transcript in the cytoplasm. Knockdown of Carlr results in impaired expression of NF-?B pathway genes and influences the interaction between macrophages and intestinal cells in an inflammatory environment. In human celiac disease patient samples, increased levels of the Carlr transcript were detected in the cytoplasm, alongside elevated expression of NF-?B pathway genes. These findings suggest that increased Carlr expression and/or cytoplasmic localization is required for efficient NF-?B signaling and is associated with the inflamed tissue state observed in human celiac disease. |*Gene Expression Regulation [MESH] |Animals [MESH] |Apoptosis [MESH] |Celiac Disease/immunology/metabolism [MESH] |Cytoplasm/*genetics/immunology/metabolism [MESH] |Gene Expression [MESH] |Humans [MESH] |Inflammation [MESH] |Intestinal Mucosa/immunology/metabolism [MESH] |Macrophages/immunology/metabolism [MESH] |Mice [MESH] |NF-kappa B/*genetics/immunology/*metabolism [MESH] |Phosphorylation [MESH] |RNA, Long Noncoding/*genetics [MESH]Cytoplasmic Form of Carlr lncRNA Facilitates Inflammatory Gene Express(epmc).pdf DeepDyve Pubget Overpricing