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10.1074/jbc.M116.744631 http://scihub22266oqcxt.onion/10.1074/jbc.M116.744631 C5076512!5076512 !27462075     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27462075 &cmd=llinks): Failed to open stream: HTTP request failed! 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Transforming Growth Factor-? (TGF-?) Inhibits the Expression of Factor VII-activating Protease (FSAP) in Hepatocytes |pdf=|usr=}}{{27462075 }} gab.com Text Transforming Growth Factor- (TGF- ) Inhibits the Expression of Factor VII-activating Protease (FSAP) in Hepatocytes JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27462075 #FOAvip Deletion of the Habp2 gene encoding Factor VII-activating protease (FSAP) increases liver fibrosis in mice. A single nucleotide polymorphism (G534E) in HABP2 leads to lower enzymatic activity and is associated with enhanced liver fibrosis in humans. Liver fibrosis is associated with a decrease in FSAP expression but, to date, nothing is known about how this might be regulated. Primary mouse hepatocytes or the hepatocyte cell line, AML12, were treated with different factors, and expression of FSAP was determined. Of the various regulatory factors tested, only transforming growth factor-? (TGF-?) demonstrated a concentration- and time-dependent inhibition of FSAP expression at the mRNA and protein level. The TGF-?-Type I receptor (ALK-5) antagonist SB431542 and Smad2 siRNA, but neither SIS3, which inhibits SMAD3, nor siRNA against Smad3 could block this effect. Various regions of the HABP2 promoter region were cloned into reporter constructs, and the promoter activity was determined. Accordingly, the promoter activity, which could phenocopy changes in Habp2 mRNA in response to TGF-?, was found to be located in the 177-bp region upstream of the transcription start site, and this region did not contain any SMAD binding sites. Mutation analysis of the promoter and chromatin immunoprecipitation assays were performed to identify an important role for the ATF3 binding element. Thus, TGF-? is the most likely mediator responsible for the decrease in FSAP expression in liver fibrosis. Twit Text FOAVip Transforming Growth Factor- (TGF- ) Inhibits the Expression of Factor VII-activating Protease (FSAP) in Hepatocytes ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27462075 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27462075 #FOAvip English Wikipedia <ref>{{Cite pmid|27462075 }}</ref> Transforming Growth Factor-? (TGF-?) Inhibits the Expression of Factor VII-activating Protease (FSAP) in Hepatocytes #MMPMID27462075 Leiting S ; Seidl S ; Martinez-Palacian A ; Muhl L ; Kanse SM J Biol Chem 2016[Sep]; 291 (40 ): 21020-21028 PMID27462075 show ga Deletion of the Habp2 gene encoding Factor VII-activating protease (FSAP) increases liver fibrosis in mice. A single nucleotide polymorphism (G534E) in HABP2 leads to lower enzymatic activity and is associated with enhanced liver fibrosis in humans. Liver fibrosis is associated with a decrease in FSAP expression but, to date, nothing is known about how this might be regulated. Primary mouse hepatocytes or the hepatocyte cell line, AML12, were treated with different factors, and expression of FSAP was determined. Of the various regulatory factors tested, only transforming growth factor-? (TGF-?) demonstrated a concentration- and time-dependent inhibition of FSAP expression at the mRNA and protein level. The TGF-?-Type I receptor (ALK-5) antagonist SB431542 and Smad2 siRNA, but neither SIS3, which inhibits SMAD3, nor siRNA against Smad3 could block this effect. Various regions of the HABP2 promoter region were cloned into reporter constructs, and the promoter activity was determined. Accordingly, the promoter activity, which could phenocopy changes in Habp2 mRNA in response to TGF-?, was found to be located in the 177-bp region upstream of the transcription start site, and this region did not contain any SMAD binding sites. Mutation analysis of the promoter and chromatin immunoprecipitation assays were performed to identify an important role for the ATF3 binding element. Thus, TGF-? is the most likely mediator responsible for the decrease in FSAP expression in liver fibrosis. |*Gene Expression Regulation, Enzymologic [MESH] |Activating Transcription Factor 3/genetics/metabolism [MESH] |Animals [MESH] |Cell Line [MESH] |Hepatocytes/*metabolism/pathology [MESH] |Humans [MESH] |Liver Cirrhosis/genetics/*metabolism/pathology [MESH] |Mice [MESH] |Protein Serine-Threonine Kinases/genetics/metabolism [MESH] |Receptor, Transforming Growth Factor-beta Type I [MESH] |Receptors, Transforming Growth Factor beta/genetics/metabolism [MESH] |Response Elements [MESH] |Serine Endopeptidases/*biosynthesis/genetics [MESH] |Smad Proteins/genetics/metabolism [MESH] |Smad3 Protein/genetics/metabolism [MESH]Transforming Growth Factor-? (TGF-?) Inhibits the Expression of Factor(epmc).pdf DeepDyve Pubget Overpricing