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10.1038/nature14508 http://scihub22266oqcxt.onion/10.1038/nature14508 C4783869!4783869!26083752     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26083752&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 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       Nature 2015 ; 522 (7557): 444-9 Nephropedia Template TP {{tp|p=26083752|t=2015. HIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart disease |pdf=|usr=}}{{26083752}} gab.com Text HIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart disease JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=26083752 #FOAvip Fructose is a major component of dietary sugar and its overconsumption exacerbates key pathological features of metabolic syndrome. The central fructose-metabolising enzyme is ketohexokinase (KHK), which exists in two isoforms: KHK-A and KHK-C, generated through mutually exclusive alternative splicing of KHK pre-mRNAs. KHK-C displays superior affinity for fructose compared with KHK-A and is produced primarily in the liver, thus restricting fructose metabolism almost exclusively to this organ. Here we show that myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1? (HIF1?) activation of SF3B1 and SF3B1-mediated splice switching of KHK-A to KHK-C. Heart-specific depletion of SF3B1 orgenetic ablation of Khk, but not Khk-A alone, in mice, suppresses pathological stress-induced fructose metabolism, growth and contractile dysfunction, thus defining signalling components and molecular underpinnings of a fructose metabolism regulatory system crucial for pathological growth. Twit Text FOAVip HIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart disease ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=26083752 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26083752 #FOAvip English Wikipedia <ref>{{Cite pmid|26083752}}</ref> HIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart disease #MMPMID26083752 Mirtschink P; Krishnan J; Grimm F; Sarre A; Hörl M; Kayikci M; Fankhauser N; Christinat Y; Cortijo C; Feehan O; Vukolic A; Sossalla S; Stehr SN; Ule J; Zamboni N; Pedrazzini T; Krek W Nature 2015[Jun]; 522 (7557): 444-9 PMID26083752show ga Fructose is a major component of dietary sugar and its overconsumption exacerbates key pathological features of metabolic syndrome. The central fructose-metabolising enzyme is ketohexokinase (KHK), which exists in two isoforms: KHK-A and KHK-C, generated through mutually exclusive alternative splicing of KHK pre-mRNAs. KHK-C displays superior affinity for fructose compared with KHK-A and is produced primarily in the liver, thus restricting fructose metabolism almost exclusively to this organ. Here we show that myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1? (HIF1?) activation of SF3B1 and SF3B1-mediated splice switching of KHK-A to KHK-C. Heart-specific depletion of SF3B1 orgenetic ablation of Khk, but not Khk-A alone, in mice, suppresses pathological stress-induced fructose metabolism, growth and contractile dysfunction, thus defining signalling components and molecular underpinnings of a fructose metabolism regulatory system crucial for pathological growth. äHIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart diseas(epmc).pdf DeepDyve Pubget Overpricing