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10.5527/wjn.v4.i3.363 http://scihub22266oqcxt.onion/10.5527/wjn.v4.i3.363 C4491926!4491926!26167459     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26167459&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       World+J+Nephrol 2015 ; 4 (3): 363-6 Nephropedia Template TP {{tp|p=26167459|t=2015. Epigenetics of epithelial Na+ channel-dependent sodium uptake and blood pressure regulation |pdf=|usr=}}{{26167459}} gab.com Text Epigenetics of epithelial Na+ channel-dependent sodium uptake and blood pressure regulation JO: World J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26167459 #FOAvip The epithelial Na+ channel (ENaC) consists of ?, ?, ? subunits. Its expression and function are regulated by aldosterone at multiple levels including transcription. ENaC plays a key role in Na+ homeostasis and blood pressure. Mutations in ENaC subunit genes result in hypertension or hypotension, depending on the nature of the mutations. Transcription of ?ENaC is considered as the rate-limiting step in the formation of functional ENaC. As an aldosterone target gene, ?ENaC is activated upon aldosterone- mineralocorticoid receptor binding to the cis-elements in the ?ENaC promoter, which is packed into chromatin. However, how aldosterone alters chromatin structure to induce changes in transcription is poorly understood. Studies by others and us suggest that Dot1a-Af9 complex represses ?ENaC by directly binding and regulating targeted histone H3 K79 hypermethylation at the specific subregions of ?ENaC promoter. Aldosterone decreases Dot1a-Af9 formation by impairing expression of Dot1a and Af9 and by inducing Sgk1, which, in turn, phosphorylates Af9 at S435 to weaken Dot1a-Af9 interaction. MR attenuates Dot1a-Af9 effect by competing with Dot1a for binding Af9. Af17 relieves repression by interfering with Dot1a-Af9 interaction and promoting Dot1a nuclear export. Af17-/- mice exhibit defects in ENaC expression, renal Na+ retention, and blood pressure control. This review gives a brief summary of these novel findings. Twit Text FOAVip Epigenetics of epithelial Na+ channel-dependent sodium uptake and blood pressure regulation ????World J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26167459 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26167459 #FOAvip English Wikipedia <ref>{{Cite pmid|26167459}}</ref> Epigenetics of epithelial Na+ channel-dependent sodium uptake and blood pressure regulation #MMPMID26167459 Zhang W World J Nephrol 2015[Jul]; 4 (3): 363-6 PMID26167459show ga The epithelial Na+ channel (ENaC) consists of ?, ?, ? subunits. Its expression and function are regulated by aldosterone at multiple levels including transcription. ENaC plays a key role in Na+ homeostasis and blood pressure. Mutations in ENaC subunit genes result in hypertension or hypotension, depending on the nature of the mutations. Transcription of ?ENaC is considered as the rate-limiting step in the formation of functional ENaC. As an aldosterone target gene, ?ENaC is activated upon aldosterone- mineralocorticoid receptor binding to the cis-elements in the ?ENaC promoter, which is packed into chromatin. However, how aldosterone alters chromatin structure to induce changes in transcription is poorly understood. Studies by others and us suggest that Dot1a-Af9 complex represses ?ENaC by directly binding and regulating targeted histone H3 K79 hypermethylation at the specific subregions of ?ENaC promoter. Aldosterone decreases Dot1a-Af9 formation by impairing expression of Dot1a and Af9 and by inducing Sgk1, which, in turn, phosphorylates Af9 at S435 to weaken Dot1a-Af9 interaction. MR attenuates Dot1a-Af9 effect by competing with Dot1a for binding Af9. Af17 relieves repression by interfering with Dot1a-Af9 interaction and promoting Dot1a nuclear export. Af17-/- mice exhibit defects in ENaC expression, renal Na+ retention, and blood pressure control. This review gives a brief summary of these novel findings. äEpigenetics of epithelial Na+ channel-dependent sodium uptake and bloo(epmc).pdf DeepDyve Pubget Overpricing