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• W2026941176 abstract "Hepatic steatosis and liver degeneration are prominent features of the zebrafish ducttrip (dtp) mutant phenotype. Positional cloning identified a causative mutation in the gene encoding S-adenosylhomocysteine hydrolase (Ahcy). Reduced Ahcy activity in dtp mutants led to elevated levels of S-adenosylhomocysteine (SAH) and, to a lesser degree, of its metabolic precursor S-adenosylmethionine (SAM). Elevated SAH in dtp larvae was associated with mitochondrial defects and increased expression of tnfa and pparg, an ortholog of the mammalian lipogenic gene. Antisense knockdown of tnfa rescued hepatic steatosis and liver degeneration in dtp larvae, whereas the overexpression of tnfa and the hepatic phenotype were unchanged in dtp larvae reared under germ-free conditions. These data identify an essential role for tnfa in the mutant phenotype and suggest a direct link between SAH-induced methylation defects and TNF expression in human liver disorders associated with elevated TNFalpha. Although heterozygous dtp larvae had no discernible phenotype, hepatic steatosis was present in heterozygous adult dtp fish and in wild-type adult fish treated with an Ahcy inhibitor. These data argue that AHCY polymorphisms and AHCY inhibitors, which have shown promise in treating autoimmunity and other disorders, may be a risk factor for steatosis, particularly in patients with diabetes, obesity and liver disorders such as hepatitis C infection. Supporting this idea, hepatic injury and steatosis have been noted in patients with recently discovered AHCY mutations." @default.
• W2026941176 created "2016-06-24" @default.
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• W2026941176 date "2009-03-01" @default.
• W2026941176 modified "2023-10-01" @default.
• W2026941176 title "TNFα-dependent hepatic steatosis and liver degeneration caused by mutation of zebrafish <i>s-adenosylhomocysteine hydrolase</i>" @default.
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• W2026941176 cites W1716248674 @default.
• W2026941176 cites W1964639766 @default.
• W2026941176 cites W1969584616 @default.
• W2026941176 cites W1972731253 @default.
• W2026941176 cites W1973833585 @default.
• W2026941176 cites W1976428197 @default.
• W2026941176 cites W1977937919 @default.
• W2026941176 cites W1980297653 @default.
• W2026941176 cites W1983880125 @default.
• W2026941176 cites W1987815797 @default.
• W2026941176 cites W1988936830 @default.
• W2026941176 cites W1989535259 @default.
• W2026941176 cites W1990810555 @default.
• W2026941176 cites W1997039338 @default.
• W2026941176 cites W2001149454 @default.
• W2026941176 cites W2001858515 @default.
• W2026941176 cites W2004160850 @default.
• W2026941176 cites W2004842870 @default.
• W2026941176 cites W2006435867 @default.
• W2026941176 cites W2008735740 @default.
• W2026941176 cites W2015376110 @default.
• W2026941176 cites W2016638697 @default.
• W2026941176 cites W2018508622 @default.
• W2026941176 cites W2019185659 @default.
• W2026941176 cites W2019296316 @default.
• W2026941176 cites W2028386875 @default.
• W2026941176 cites W2029469992 @default.
• W2026941176 cites W2031308714 @default.
• W2026941176 cites W2036862601 @default.
• W2026941176 cites W2037149610 @default.
• W2026941176 cites W2044318948 @default.
• W2026941176 cites W2044682380 @default.
• W2026941176 cites W2048619491 @default.
• W2026941176 cites W2049713116 @default.
• W2026941176 cites W2051019972 @default.
• W2026941176 cites W2051525362 @default.
• W2026941176 cites W2055243017 @default.
• W2026941176 cites W2055448579 @default.
• W2026941176 cites W2056897523 @default.
• W2026941176 cites W2065157394 @default.
• W2026941176 cites W2068975363 @default.
• W2026941176 cites W2070053386 @default.
• W2026941176 cites W2072780015 @default.
• W2026941176 cites W2074354128 @default.
• W2026941176 cites W2084789101 @default.
• W2026941176 cites W2088555721 @default.
• W2026941176 cites W2089401171 @default.
• W2026941176 cites W2089764511 @default.
• W2026941176 cites W2094998344 @default.
• W2026941176 cites W2099536385 @default.
• W2026941176 cites W2102520758 @default.
• W2026941176 cites W2108324688 @default.
• W2026941176 cites W2110029891 @default.
• W2026941176 cites W2113634596 @default.
• W2026941176 cites W2114277691 @default.
• W2026941176 cites W2117889142 @default.
• W2026941176 cites W2117954751 @default.
• W2026941176 cites W2118428501 @default.
• W2026941176 cites W2122500634 @default.
• W2026941176 cites W2123552387 @default.
• W2026941176 cites W2127281349 @default.
• W2026941176 cites W2128171794 @default.
• W2026941176 cites W2132739516 @default.
• W2026941176 cites W2141158324 @default.
• W2026941176 cites W2141710362 @default.
• W2026941176 cites W2145750252 @default.
• W2026941176 cites W2154234231 @default.
• W2026941176 cites W2164017272 @default.
• W2026941176 cites W2165002886 @default.
• W2026941176 cites W2412554695 @default.
• W2026941176 cites W4230280576 @default.
• W2026941176 cites W4241311067 @default.
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• W2026941176 doi "https://doi.org/10.1242/dev.027565" @default.
• W2026941176 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2685951" @default.
• W2026941176 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19201949" @default.
• W2026941176 hasPublicationYear "2009" @default.
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