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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The acute phase response is associated with retinoid X receptor repression in rodent liver.
TL;DR: It is demonstrated that lipopolysaccharide (LPS) induces a rapid, dose-dependent decrease in RXRα, RXRβ, and RXRγ proteins in hamster liver, and increased RNA degradation is likely responsible for the repression of RXR.
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Peroxisome Proliferator-Activated Receptor (PPAR)-β/δ Stimulates Differentiation and Lipid Accumulation in Keratinocytes
Matthias Schmuth,Christopher M. Haqq,William Cairns,Julie C. Holder,Sheri T. Dorsam,Sandra Chang,Peggy Lau,Ashley J. Fowler,Gary Chuang,Arthur H. Moser,Barbara E. Brown,Man Mao-Qiang,Yoshikazu Uchida,Kristina Schoonjans,Johan Auwerx,Pierre Chambon,Timothy M. Willson,Peter M. Elias,Kenneth R. Feingold +18 more
TL;DR: Together, these studies indicate that PPAR-beta/delta activation stimulates keratinocyte differentiation, is anti-inflammatory, improves barrier homeostasis, and stimulates TG accumulation in keratinocytes.
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De novo sterologenesis in the skin. II. Regulation by cutaneous barrier requirements.
TL;DR: The results suggest that maintenance of barrier function is one purpose of epidermal de novo nonsaponifiable lipid synthesis, and demonstrate further that, despite a lack of low density lipoprotein receptors, epidermis can regulate its lipid-synthetic apparatus in response to certain specific requirements.
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Infection and Inflammation Induce LDL Oxidation In Vivo
Riaz A. Memon,Ilona Staprans,Mustafa A. Noor,Walter M. Holleran,Yoshikazu Uchida,Arthur H. Moser,Kenneth R. Feingold,Carl Grunfeld +7 more
TL;DR: Results demonstrate that the host response to infection and inflammation increases oxidized lipids in serum and induces LDL oxidation in vivo, which may promote atherogenesis and could be a mechanism for increased incidence of coronary artery disease in patients with chronic infections and inflammatory disorders.
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Mechanisms of triglyceride accumulation in activated macrophages
Kenneth R. Feingold,Judy K. Shigenaga,Mahmood R. Kazemi,Carol M. McDonald,Sophie Patzek,Andrew S. Cross,Arthur H. Moser,Carl Grunfeld +7 more
TL;DR: Activation of TLRs leads to accumulation of TG in macrophages by multiple pathways that may have beneficial effects in host defense but could contribute to the accelerated atherosclerosis in chronic infections and inflammatory diseases.