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10.1074/jbc.M115.709386 http://scihub22266oqcxt.onion/10.1074/jbc.M115.709386 C4933239!4933239 !27129775     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27129775 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cofactors of LIM Domains Associate with Estrogen Receptor ? to Regulate the Expression of Noncoding RNA H19 and Corneal Epithelial Progenitor Cell Function |pdf=|usr=}}{{27129775 }} gab.com Text Cofactors of LIM Domains Associate with Estrogen Receptor to Regulate the Expression of Noncoding RNA H19 and Corneal Epithelial Progenitor Cell Function JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27129775 #FOAvip Cofactors of LIM domain proteins, CLIM1 and CLIM2, are widely expressed transcriptional cofactors that are recruited to gene regulatory regions by DNA-binding proteins, including LIM domain transcription factors. In the cornea, epithelium-specific expression of a dominant negative (DN) CLIM under the keratin 14 (K14) promoter causes blistering, wounding, inflammation, epithelial hyperplasia, and neovascularization followed by epithelial thinning and subsequent epidermal-like differentiation of the corneal epithelium. The defects in corneal epithelial differentiation and cell fate determination suggest that CLIM may regulate corneal progenitor cells and the transition to differentiation. Consistent with this notion, the K14-DN-Clim corneal epithelium first exhibits increased proliferation followed by fewer progenitor cells with decreased proliferative potential. In vivo ChIP-sequencing experiments with corneal epithelium show that CLIM binds to and regulates numerous genes involved in cell adhesion and proliferation, including limbally enriched genes. Intriguingly, CLIM associates primarily with non-LIM homeodomain motifs in corneal epithelial cells, including that of estrogen receptor ?. Among CLIM targets is the noncoding RNA H19 whose deregulation is associated with Silver-Russell and Beckwith-Wiedemann syndromes. We demonstrate here that H19 negatively regulates corneal epithelial proliferation. In addition to cell cycle regulators, H19 affects the expression of multiple cell adhesion genes. CLIM interacts with estrogen receptor ? at the H19 locus, potentially explaining the higher expression of H19 in female than male corneas. Together, our results demonstrate an important role for CLIM in regulating the proliferative potential of corneal epithelial progenitors and identify CLIM downstream target H19 as a regulator of corneal epithelial proliferation and adhesion. Twit Text FOAVip Cofactors of LIM Domains Associate with Estrogen Receptor to Regulate the Expression of Noncoding RNA H19 and Corneal Epithelial Progenitor Cell Function ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27129775 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27129775 #FOAvip English Wikipedia <ref>{{Cite pmid|27129775 }}</ref> Cofactors of LIM Domains Associate with Estrogen Receptor ? to Regulate the Expression of Noncoding RNA H19 and Corneal Epithelial Progenitor Cell Function #MMPMID27129775 Klein RH ; Stephens DN ; Ho H ; Chen JK ; Salmans ML ; Wang W ; Yu Z ; Andersen B J Biol Chem 2016[Jun]; 291 (25 ): 13271-85 PMID27129775 show ga Cofactors of LIM domain proteins, CLIM1 and CLIM2, are widely expressed transcriptional cofactors that are recruited to gene regulatory regions by DNA-binding proteins, including LIM domain transcription factors. In the cornea, epithelium-specific expression of a dominant negative (DN) CLIM under the keratin 14 (K14) promoter causes blistering, wounding, inflammation, epithelial hyperplasia, and neovascularization followed by epithelial thinning and subsequent epidermal-like differentiation of the corneal epithelium. The defects in corneal epithelial differentiation and cell fate determination suggest that CLIM may regulate corneal progenitor cells and the transition to differentiation. Consistent with this notion, the K14-DN-Clim corneal epithelium first exhibits increased proliferation followed by fewer progenitor cells with decreased proliferative potential. In vivo ChIP-sequencing experiments with corneal epithelium show that CLIM binds to and regulates numerous genes involved in cell adhesion and proliferation, including limbally enriched genes. Intriguingly, CLIM associates primarily with non-LIM homeodomain motifs in corneal epithelial cells, including that of estrogen receptor ?. Among CLIM targets is the noncoding RNA H19 whose deregulation is associated with Silver-Russell and Beckwith-Wiedemann syndromes. We demonstrate here that H19 negatively regulates corneal epithelial proliferation. In addition to cell cycle regulators, H19 affects the expression of multiple cell adhesion genes. CLIM interacts with estrogen receptor ? at the H19 locus, potentially explaining the higher expression of H19 in female than male corneas. Together, our results demonstrate an important role for CLIM in regulating the proliferative potential of corneal epithelial progenitors and identify CLIM downstream target H19 as a regulator of corneal epithelial proliferation and adhesion. |Animals [MESH] |Cell Adhesion [MESH] |Cell Adhesion Molecules/genetics/metabolism [MESH] |Cell Proliferation [MESH] |DNA-Binding Proteins/*metabolism [MESH] |Epithelial Cells/*physiology [MESH] |Epithelium, Corneal/cytology [MESH] |Estrogen Receptor alpha/*metabolism [MESH] |Female [MESH] |Gene Expression Regulation [MESH] |Humans [MESH] |LIM Domain Proteins/*metabolism [MESH] |Male [MESH] |Mice, Transgenic [MESH] |RNA, Long Noncoding/*genetics/metabolism [MESH] |Stem Cells/*physiology [MESH]Cofactors of LIM Domains Associate with Estrogen Receptor ? to Regulat(epmc).pdf DeepDyve Pubget Overpricing