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10.3390/cancers10060183 http://scihub22266oqcxt.onion/10.3390/cancers10060183 C6025395!6025395!29874844     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29874844&cmd=llinks): Failed to open stream: HTTP request failed! 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Clinico-Pathological Importance of TGF-?/Phospho-Smad Signaling during Human Hepatic Fibrocarcinogenesis |pdf=|usr=}}{{29874844}} gab.com Text Clinico-Pathological Importance of TGF- /Phospho-Smad Signaling during Human Hepatic Fibrocarcinogenesis JO: Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=29874844 #FOAvip Chronic viral hepatitis is a global public health problem, with approximately 570 million persons chronically infected. Hepatitis B and C viruses increase the risk of morbidity and mortality from liver cirrhosis, hepatocellular carcinoma (HCC), and extrahepatic complications that develop. Hepatitis virus infection induces transforming growth factor (TGF)-?, which influences microenvironments within the infected liver. TGF-? promotes liver fibrosis by up-regulating extracellular matrix production by hepatic stellate cells. TGF-? is also up-regulated in patients with HCC, in whom it contributes importantly to bringing about a favorable microenvironment for tumor growth. Thus, TGF-? is thought to be a major factor regulating liver fibrosis and carcinogenesis. Since TGF-? carries out regulatory signaling by influencing the phosphorylation of Smads, we have generated several kinds of phospho-specific antibodies to Smad2/3. Using these, we have identified three types of phospohorylated forms: COOH-terminally phosphorylated Smad2/3 (pSmad2C and pSmad3C), linker phosphorylated Smad2/3 (pSmad2L and pSmad3L), and dually phosphorylated Smad3 (pSmad2L/C and pSmad3L/C). TGF-?-mediated pSmad2/3C signaling terminates cell proliferation; on the other hand, cytokine-induced pSmad3L signaling accelerates cell proliferation and promotes fibrogenesis. This review addresses TGF-?/Smad signal transduction in chronic liver injuries and carcinogenic processes. We also discuss the reversibility of Smad signaling after antiviral therapy. Twit Text FOAVip Clinico-Pathological Importance of TGF- /Phospho-Smad Signaling during Human Hepatic Fibrocarcinogenesis ????Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=29874844 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29874844 #FOAvip English Wikipedia <ref>{{Cite pmid|29874844}}</ref> Clinico-Pathological Importance of TGF-?/Phospho-Smad Signaling during Human Hepatic Fibrocarcinogenesis #MMPMID29874844 Yoshida K; Matsuzaki K; Murata M; Yamaguchi T; Suwa K; Okazaki K Cancers (Basel) 2018[Jun]; 10 (6): ä PMID29874844show ga Chronic viral hepatitis is a global public health problem, with approximately 570 million persons chronically infected. Hepatitis B and C viruses increase the risk of morbidity and mortality from liver cirrhosis, hepatocellular carcinoma (HCC), and extrahepatic complications that develop. Hepatitis virus infection induces transforming growth factor (TGF)-?, which influences microenvironments within the infected liver. TGF-? promotes liver fibrosis by up-regulating extracellular matrix production by hepatic stellate cells. TGF-? is also up-regulated in patients with HCC, in whom it contributes importantly to bringing about a favorable microenvironment for tumor growth. Thus, TGF-? is thought to be a major factor regulating liver fibrosis and carcinogenesis. Since TGF-? carries out regulatory signaling by influencing the phosphorylation of Smads, we have generated several kinds of phospho-specific antibodies to Smad2/3. Using these, we have identified three types of phospohorylated forms: COOH-terminally phosphorylated Smad2/3 (pSmad2C and pSmad3C), linker phosphorylated Smad2/3 (pSmad2L and pSmad3L), and dually phosphorylated Smad3 (pSmad2L/C and pSmad3L/C). TGF-?-mediated pSmad2/3C signaling terminates cell proliferation; on the other hand, cytokine-induced pSmad3L signaling accelerates cell proliferation and promotes fibrogenesis. This review addresses TGF-?/Smad signal transduction in chronic liver injuries and carcinogenic processes. We also discuss the reversibility of Smad signaling after antiviral therapy. äClinico-Pathological Importance of TGF-?/Phospho-Smad Signaling during(epmc).pdf DeepDyve Pubget Overpricing