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10.1074/jbc.M115.691543 http://scihub22266oqcxt.onion/10.1074/jbc.M115.691543 C4933231!4933231!27129231     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2016 ; 291 (25): 13160-74 Nephropedia Template TP {{tp|p=27129231|t=2016. Transforming Growth Factor ?1 (TGF-?1) Activates Hepcidin mRNA Expression in Hepatocytes* |pdf=|usr=}}{{27129231}} gab.com Text Transforming Growth Factor 1 (TGF- 1) Activates Hepcidin mRNA Expression in Hepatocytes* JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27129231 #FOAvip The hepatic hormone hepcidin is the master regulator of systemic iron homeostasis. Its expression level is adjusted to alterations in iron levels, inflammatory cues, and iron requirements for erythropoiesis. Bone morphogenetic protein 6 (BMP6) contributes to the iron-dependent control of hepcidin. In addition, TGF-?1 may stimulate hepcidin mRNA expression in murine hepatocytes and human leukocytes. However, receptors and downstream signaling proteins involved in TGF-?1-induced hepcidin expression are still unclear. Here we show that TGF-?1 treatment of mouse and human hepatocytes, as well as ectopic expression of TGF-?1 in mice, increases hepcidin mRNA levels. The hepcidin response to TGF-?1 depends on functional TGF-?1 type I receptor (ALK5) and TGF-?1 type II receptor (T?RII) and is mediated by a noncanonical mechanism that involves Smad1/5/8 phosphorylation. Interestingly, increasing availability of canonical Smad2/3 decreases TGF-?1-induced hepcidin regulation, whereas the BMP6-hepcidin signal was enhanced, indicating a signaling component stoichiometry-dependent cross-talk between the two pathways. Although ALK2/3-dependent hepcidin activation by BMP6 can be modulated by each of the three hemochromatosis-associated proteins: HJV (hemojuvelin), HFE (hemochromatosis protein), and TfR2 (transferrin receptor 2), these proteins do not control the ALK5-mediated hepcidin response to TGF-?1. TGF-?1 mRNA levels are increased in mouse models of iron overload, indicating that TGF-?1 may contribute to hepcidin synthesis under these conditions. In conclusion, these data demonstrate that a complex regulatory network involving TGF-?1 and BMP6 may control the sensing of systemic and/or hepatic iron levels. Twit Text FOAVip Transforming Growth Factor 1 (TGF- 1) Activates Hepcidin mRNA Expression in Hepatocytes* ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27129231 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27129231 #FOAvip English Wikipedia <ref>{{Cite pmid|27129231}}</ref> Transforming Growth Factor ?1 (TGF-?1) Activates Hepcidin mRNA Expression in Hepatocytes* #MMPMID27129231 Chen S; Feng T; Vuji? Spasi? M; Altamura S; Breitkopf-Heinlein K; Altenöder J; Weiss TS; Dooley S; Muckenthaler MU J Biol Chem 2016[Jun]; 291 (25): 13160-74 PMID27129231show ga The hepatic hormone hepcidin is the master regulator of systemic iron homeostasis. Its expression level is adjusted to alterations in iron levels, inflammatory cues, and iron requirements for erythropoiesis. Bone morphogenetic protein 6 (BMP6) contributes to the iron-dependent control of hepcidin. In addition, TGF-?1 may stimulate hepcidin mRNA expression in murine hepatocytes and human leukocytes. However, receptors and downstream signaling proteins involved in TGF-?1-induced hepcidin expression are still unclear. Here we show that TGF-?1 treatment of mouse and human hepatocytes, as well as ectopic expression of TGF-?1 in mice, increases hepcidin mRNA levels. The hepcidin response to TGF-?1 depends on functional TGF-?1 type I receptor (ALK5) and TGF-?1 type II receptor (T?RII) and is mediated by a noncanonical mechanism that involves Smad1/5/8 phosphorylation. Interestingly, increasing availability of canonical Smad2/3 decreases TGF-?1-induced hepcidin regulation, whereas the BMP6-hepcidin signal was enhanced, indicating a signaling component stoichiometry-dependent cross-talk between the two pathways. Although ALK2/3-dependent hepcidin activation by BMP6 can be modulated by each of the three hemochromatosis-associated proteins: HJV (hemojuvelin), HFE (hemochromatosis protein), and TfR2 (transferrin receptor 2), these proteins do not control the ALK5-mediated hepcidin response to TGF-?1. TGF-?1 mRNA levels are increased in mouse models of iron overload, indicating that TGF-?1 may contribute to hepcidin synthesis under these conditions. In conclusion, these data demonstrate that a complex regulatory network involving TGF-?1 and BMP6 may control the sensing of systemic and/or hepatic iron levels. äTransforming Growth Factor ?1 (TGF-?1) Activates Hepcidin mRNA Express(epmc).pdf DeepDyve Pubget Overpricing