Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/ncomms6797 http://scihub22266oqcxt.onion/10.1038/ncomms6797 C4268882!4268882!25504335     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2014 ; 5 (ä): 5797 Nephropedia Template TP {{tp|p=25504335|t=2014. Simultaneous downregulation of KLF5 and Fli1 is a key feature underlying systemic sclerosis |pdf=|usr=}}{{25504335}} gab.com Text Simultaneous downregulation of KLF5 and Fli1 is a key feature underlying systemic sclerosis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25504335 #FOAvip Systemic sclerosis (SSc) is manifested by fibrosis, vasculopathy and immune dysregulation. So far, a unifying hypothesis underpinning these pathological events remains unknown. Given that SSc is a multifactorial disease caused by both genetic and environmental factors, we focus on the two transcription factors, which modulate the fibrotic reaction and are epigenetically suppressed in SSc dermal fibroblasts, Friend leukemia integration 1 (Fli1) and Krüppel-like factor 5 (KLF5). In addition to Fli1 silencing-dependent collagen induction, simultaneous knockdown of Fli1 and KLF5 synergistically enhances expression of connective tissue growth factor. Notably, mice with double heterozygous deficiency of Klf5 and Fli1 mimicking the epigenetic phenotype of SSc skin spontaneously recapitulate all the three features of SSc, including fibrosis and vasculopathy of the skin and lung, B cell activation, and autoantibody production. These studies implicate the epigenetic downregulation of Fli1 and KLF5 as a central event triggering the pathogenic triad of SSc. Twit Text FOAVip Simultaneous downregulation of KLF5 and Fli1 is a key feature underlying systemic sclerosis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25504335 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25504335 #FOAvip English Wikipedia <ref>{{Cite pmid|25504335}}</ref> Simultaneous downregulation of KLF5 and Fli1 is a key feature underlying systemic sclerosis #MMPMID25504335 Noda S; Asano Y; Nishimura S; Taniguchi T; Fujiu K; Manabe I; Nakamura K; Yamashita T; Saigusa R; Akamata K; Takahashi T; Ichimura Y; Toyama T; Tsuruta D; Trojanowska M; Nagai R; Sato S Nat Commun 2014[]; 5 (ä): 5797 PMID25504335show ga Systemic sclerosis (SSc) is manifested by fibrosis, vasculopathy and immune dysregulation. So far, a unifying hypothesis underpinning these pathological events remains unknown. Given that SSc is a multifactorial disease caused by both genetic and environmental factors, we focus on the two transcription factors, which modulate the fibrotic reaction and are epigenetically suppressed in SSc dermal fibroblasts, Friend leukemia integration 1 (Fli1) and Krüppel-like factor 5 (KLF5). In addition to Fli1 silencing-dependent collagen induction, simultaneous knockdown of Fli1 and KLF5 synergistically enhances expression of connective tissue growth factor. Notably, mice with double heterozygous deficiency of Klf5 and Fli1 mimicking the epigenetic phenotype of SSc skin spontaneously recapitulate all the three features of SSc, including fibrosis and vasculopathy of the skin and lung, B cell activation, and autoantibody production. These studies implicate the epigenetic downregulation of Fli1 and KLF5 as a central event triggering the pathogenic triad of SSc. äSimultaneous downregulation of KLF5 and Fli1 is a key feature underlyi(epmc).pdf DeepDyve Pubget Overpricing