scispace - formally typeset
D

Daniel H. Hwang

Researcher at University of California, Davis

Publications -  94
Citations -  13581

Daniel H. Hwang is an academic researcher from University of California, Davis. The author has contributed to research in topics: Signal transduction & Proinflammatory cytokine. The author has an hindex of 51, co-authored 88 publications receiving 12632 citations. Previous affiliations of Daniel H. Hwang include United States Department of Agriculture & Agricultural Research Service.

Papers
More filters
Journal ArticleDOI

Saturated fatty acids, but not unsaturated fatty acids, induce the expression of cyclooxygenase-2 mediated through Toll-like receptor 4.

TL;DR: A novel mechanism by which fatty acids modulate signaling pathways and target gene expression is represented by both SFA-induced COX-2 expression and its inhibition by UFAs are mediated through a common signaling pathway derived from Tlr4.
Journal ArticleDOI

Selective expression of mitogen-inducible cyclooxygenase in macrophages stimulated with lipopolysaccharide.

TL;DR: The results indicate that increased synthesis of prostaglandins and thromboxanes in lipopolysaccharide-stimulated macrophages results from selective expression of COX-2, a newly discovered mitogen-inducible cyclooxygenase encoded by a 4-kilobase mRNA.
Journal ArticleDOI

Serine phosphorylation of insulin receptor substrate 1 by inhibitor κB kinase complex

TL;DR: It is suggested that IRS- 1 is a novel direct substrate for IKK and that phosphorylation of IRS-1 at Ser312 (and other sites) by IKK may contribute to the insulin resistance mediated by activation of inflammatory pathways.
Journal ArticleDOI

Differential modulation of Toll-like receptors by fatty acids preferential inhibition by n-3 polyunsaturated fatty acids

TL;DR: Results demonstrate that inhibition of COX-2 expression by n-3 PUFAs is mediated through the modulation of TLR-mediated signaling pathways, and the beneficial or detrimental effects of different types of dietary fatty acids on the risk of the development of many chronic inflammatory diseases may be in part mediated throughThe modulation ofTLRs.
Journal ArticleDOI

Plasma acylcarnitine profiles suggest incomplete long-chain fatty acid β-oxidation and altered tricarboxylic acid cycle activity in type 2 diabetic African-American women.

TL;DR: Results are consistent with the working hypothesis that inefficient tissue LCFA beta-oxidation, due in part to a relatively low tricarboxylic acid cycle capacity, increases tissue accumulation of acetyl-CoA and generates chain-shortened acylcarnitine molecules that activate proinflammatory pathways implicated in insulin resistance.