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10.3390/ijms17020197 http://scihub22266oqcxt.onion/10.3390/ijms17020197 C4783931!4783931 !26848653     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26848653 &cmd=llinks): Failed to open stream: HTTP request failed! 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Apobec-1 Complementation Factor (A1CF) Inhibits Epithelial-Mesenchymal Transition and Migration of Normal Rat Kidney Proximal Tubular Epithelial Cells |pdf=|usr=}}{{26848653 }} gab.com Text Apobec-1 Complementation Factor (A1CF) Inhibits Epithelial-Mesenchymal Transition and Migration of Normal Rat Kidney Proximal Tubular Epithelial Cells JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=26848653 #FOAvip Apobec-1 complementation factor (A1CF) is a member of the heterogeneous nuclear ribonucleoproteins (hnRNP) family, which participates in site-specific posttranscriptional RNA editing of apolipoprotein B (apoB) transcript. The posttranscriptional editing of apoB mRNA by A1CF in the small intestine is required for lipid absorption. Apart from the intestine, A1CF mRNA is also reported to be highly expressed in the kidneys. However, it is remained unknown about the functions of A1CF in the kidneys. The aim of this paper is to explore the potential functions of A1CF in the kidneys. Our results demonstrated that in C57BL/6 mice A1CF was weakly expressed in embryonic kidneys from E15.5dpc while strongly expressed in mature kidneys after birth, and it mainly existed in the tubules of inner cortex. More importantly, we identified A1CF negatively regulated the process of epithelial-mesenchymal transition (EMT) in kidney tubular epithelial cells. Our results found ectopic expression of A1CF up-regulated the epithelial markers E-cadherin, and down-regulated the mesenchymal markers vimentin and ?-smooth muscle actin (?-SMA) in NRK52e cells. In addition, knockdown of A1CF enhanced EMT contrary to the overexpression effect. Notably, the two A1CF variants led to the similar trend in the EMT process. Taken together, these data suggest that A1CF may be an antagonistic factor to the EMT process of kidney tubular epithelial cells. Twit Text FOAVip Apobec-1 Complementation Factor (A1CF) Inhibits Epithelial-Mesenchymal Transition and Migration of Normal Rat Kidney Proximal Tubular Epithelial Cells ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=26848653 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26848653 #FOAvip English Wikipedia <ref>{{Cite pmid|26848653 }}</ref> Apobec-1 Complementation Factor (A1CF) Inhibits Epithelial-Mesenchymal Transition and Migration of Normal Rat Kidney Proximal Tubular Epithelial Cells #MMPMID26848653 Huang L ; Wang H ; Zhou Y ; Ni D ; Hu Y ; Long Y ; Liu J ; Peng R ; Zhou L ; Liu Z ; Lyu Z ; Mao Z ; Hao J ; Li Y ; Zhou Q Int J Mol Sci 2016[Feb]; 17 (2 ): ä PMID26848653 show ga Apobec-1 complementation factor (A1CF) is a member of the heterogeneous nuclear ribonucleoproteins (hnRNP) family, which participates in site-specific posttranscriptional RNA editing of apolipoprotein B (apoB) transcript. The posttranscriptional editing of apoB mRNA by A1CF in the small intestine is required for lipid absorption. Apart from the intestine, A1CF mRNA is also reported to be highly expressed in the kidneys. However, it is remained unknown about the functions of A1CF in the kidneys. The aim of this paper is to explore the potential functions of A1CF in the kidneys. Our results demonstrated that in C57BL/6 mice A1CF was weakly expressed in embryonic kidneys from E15.5dpc while strongly expressed in mature kidneys after birth, and it mainly existed in the tubules of inner cortex. More importantly, we identified A1CF negatively regulated the process of epithelial-mesenchymal transition (EMT) in kidney tubular epithelial cells. Our results found ectopic expression of A1CF up-regulated the epithelial markers E-cadherin, and down-regulated the mesenchymal markers vimentin and ?-smooth muscle actin (?-SMA) in NRK52e cells. In addition, knockdown of A1CF enhanced EMT contrary to the overexpression effect. Notably, the two A1CF variants led to the similar trend in the EMT process. Taken together, these data suggest that A1CF may be an antagonistic factor to the EMT process of kidney tubular epithelial cells. |*Cell Movement [MESH] |*Epithelial-Mesenchymal Transition [MESH] |Actins/genetics/metabolism [MESH] |Animals [MESH] |Cadherins/genetics/metabolism [MESH] |Cell Line [MESH] |Epithelial Cells/*metabolism/physiology [MESH] |Heterogeneous-Nuclear Ribonucleoproteins/genetics/*metabolism [MESH] |Kidney Tubules, Proximal/cytology/growth & development/*metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH]Apobec-1 Complementation Factor (A1CF) Inhibits Epithelial-Mesenchymal(epmc).pdf DeepDyve Pubget Overpricing