A
Arthur H. Moser
Researcher at University of California, San Francisco
Publications - 94
Citations - 9057
Arthur H. Moser is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Tumor necrosis factor alpha & Cholesterol. The author has an hindex of 52, co-authored 94 publications receiving 8554 citations. Previous affiliations of Arthur H. Moser include San Francisco VA Medical Center & United States Department of Veterans Affairs.
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Journal ArticleDOI
Regulation of scavenger receptor class B type I in hamster liver and Hep3B cells by endotoxin and cytokines.
Weerapan Khovidhunkit,Arthur H. Moser,Judy K. Shigenaga,Judy K. Shigenaga,Carl Grunfeld,Carl Grunfeld,Kenneth R. Feingold,Kenneth R. Feingold +7 more
TL;DR: The results suggest that the decrease in hepatic SR-BI levels due to LPS and cytokines during infection and inflammation may decrease selective uptake of cholesteryl ester into the liver and result in impaired reverse cholesterol transport.
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Sick euthyroid syndrome is associated with decreased TR expression and DNA binding in mouse liver.
TL;DR: It is proposed that decreased RXR expression is limiting for RXR/TR DNA binding at 4 h, whereas the reduction in both TR and RXR levels results in further decreased binding at 16 h.
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Localization of de novo sterologenesis in mammalian skin.
Kenneth R. Feingold,Kenneth R. Feingold,Barbara E. Brown,Barbara E. Brown,Steven R. Lear,Steven R. Lear,Arthur H. Moser,Arthur H. Moser,Peter M. Elias,Peter M. Elias +9 more
TL;DR: The aim of the present study was to localize the major sites of sterol synthesis within the skin and to determine which of these sites accounted for the sex differences in sterologenesis.
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LPS and proinflammatory cytokines decrease lipin-1 in mouse adipose tissue and 3T3-L1 adipocytes
TL;DR: It is demonstrated that expression of lipin-1, one of the essential triglyceride synthetic enzymes, was suppressed by LPS, zymosan, and proinflammatory cytokines in mouse adipose tissue and in cultured 3T3-L1 adipocytes, which could contribute to a decrease in the utilization of FFA to synthesize triglycerides in adipOSE tissue, thus promoting the release of F FA into the circulation.
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In vivo regulation of acyl-CoA synthetase mRNA and activity by endotoxin and cytokines
TL;DR: The results indicate that LPS and cytokines decrease ACS1 mRNA expression and ACS activity in tissues where FA uptake and/or oxidation is decreased during sepsis, and this may support the reesterification of peripherally derived FA for triglyceride synthesis.