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10.1152/ajpcell.00093.2014 http://scihub22266oqcxt.onion/10.1152/ajpcell.00093.2014 C4060001!4060001 !24740539     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24740539 &cmd=llinks): Failed to open stream: HTTP request failed! 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Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation by differentially modulating RNA-binding proteins HuR and CUGBP1 |pdf=|usr=}}{{24740539 }} gab.com Text Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation by differentially modulating RNA-binding proteins HuR and CUGBP1 JO: Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24740539 #FOAvip Homeostasis and maturation of the mammalian intestinal epithelium are preserved through strict regulation of cell proliferation, apoptosis, and differentiation, but the exact mechanism underlying this process remains largely unknown. c-Jun NH2-terminal kinase 2 (JNK2) is highly expressed in the intestinal mucosa, and its activation plays an important role in proliferation and also mediates apoptosis in cultured intestinal epithelial cells (IECs). Here, we investigated the in vivo function of JNK2 in the regulation of intestinal epithelial homeostasis and maturation by using a targeted gene deletion approach. Targeted deletion of the jnk2 gene increased cell proliferation within the crypts in the small intestine and disrupted mucosal maturation as indicated by decreases in the height of villi and the villus-to-crypt ratio. JNK2 deletion also decreased susceptibility of the intestinal epithelium to apoptosis. JNK2-deficient intestinal epithelium was associated with an increase in the level of the RNA-binding protein HuR and with a decrease in the abundance of CUG-binding protein 1 (CUGBP1). In studies in vitro, JNK2 silencing protected intestinal epithelial cell-6 (IEC-6) cells against apoptosis and this protection was prevented by inhibiting HuR. Ectopic overexpression of CUGBP1 repressed IEC-6 cell proliferation, whereas CUGBP1 silencing enhanced cell growth. These results indicate that JNK2 is essential for maintenance of normal intestinal epithelial homeostasis and maturation under biological conditions by differentially modulating HuR and CUGBP1. Twit Text FOAVip Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation by differentially modulating RNA-binding proteins HuR and CUGBP1 ????Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24740539 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24740539 #FOAvip English Wikipedia <ref>{{Cite pmid|24740539 }}</ref> Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation by differentially modulating RNA-binding proteins HuR and CUGBP1 #MMPMID24740539 Chung HK ; Rao JN ; Zou T ; Liu L ; Xiao L ; Gu H ; Turner DJ ; Yang P ; Wang JY Am J Physiol Cell Physiol 2014[Jun]; 306 (12 ): C1167-75 PMID24740539 show ga Homeostasis and maturation of the mammalian intestinal epithelium are preserved through strict regulation of cell proliferation, apoptosis, and differentiation, but the exact mechanism underlying this process remains largely unknown. c-Jun NH2-terminal kinase 2 (JNK2) is highly expressed in the intestinal mucosa, and its activation plays an important role in proliferation and also mediates apoptosis in cultured intestinal epithelial cells (IECs). Here, we investigated the in vivo function of JNK2 in the regulation of intestinal epithelial homeostasis and maturation by using a targeted gene deletion approach. Targeted deletion of the jnk2 gene increased cell proliferation within the crypts in the small intestine and disrupted mucosal maturation as indicated by decreases in the height of villi and the villus-to-crypt ratio. JNK2 deletion also decreased susceptibility of the intestinal epithelium to apoptosis. JNK2-deficient intestinal epithelium was associated with an increase in the level of the RNA-binding protein HuR and with a decrease in the abundance of CUG-binding protein 1 (CUGBP1). In studies in vitro, JNK2 silencing protected intestinal epithelial cell-6 (IEC-6) cells against apoptosis and this protection was prevented by inhibiting HuR. Ectopic overexpression of CUGBP1 repressed IEC-6 cell proliferation, whereas CUGBP1 silencing enhanced cell growth. These results indicate that JNK2 is essential for maintenance of normal intestinal epithelial homeostasis and maturation under biological conditions by differentially modulating HuR and CUGBP1. |Animals [MESH] |CELF1 Protein [MESH] |Cell Proliferation [MESH] |Cells, Cultured [MESH] |ELAV Proteins/antagonists & inhibitors/genetics/*metabolism [MESH] |Epithelial Cells/metabolism [MESH] |Gene Expression Regulation/genetics [MESH] |Homeostasis/genetics [MESH] |Humans [MESH] |Intestinal Mucosa/*metabolism/pathology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Mitogen-Activated Protein Kinase 9/*genetics/metabolism [MESH]Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation b(epmc).pdf DeepDyve Pubget Overpricing