scispace - formally typeset
D

David L. Silver

Researcher at National University of Singapore

Publications -  85
Citations -  17711

David L. Silver is an academic researcher from National University of Singapore. The author has contributed to research in topics: Lipid droplet & Cholesterol. The author has an hindex of 42, co-authored 75 publications receiving 6863 citations. Previous affiliations of David L. Silver include Columbia University & Max Planck Society.

Papers
More filters
Journal ArticleDOI

Mfsd2a is a transporter for the essential omega-3 fatty acid docosahexaenoic acid

TL;DR: This work identifies a member of the major facilitator superfamily—Mfsd2a (previously an orphan transporter)—as the major transporter for DHA uptake into brain and reveals an unexpected essential physiological role of plasma-derived LPCs in brain growth and function.
Journal ArticleDOI

The forkhead transcription factor Foxo1 (Fkhr) confers insulin sensitivity onto glucose-6-phosphatase expression

TL;DR: It is reported that in glucogenetic kidney epithelial cells, Pepck and G6p expression are induced by dexamethasone and cAMP, but fail to be inhibited by insulin, consistent with the possibility that Foxo1 is involved in insulin regulation of glucose production by mediating the ability of insulin to decrease the glucocorticoid/cAMP response of G 6p.
Journal ArticleDOI

Specific Binding of ApoA-I, Enhanced Cholesterol Efflux, and Altered Plasma Membrane Morphology in Cells Expressing ABC1

TL;DR: The studies provide evidence for a direct interaction between ABC1 and apoA-I, but not HDL, indicating that free apoB-I is the metabolic substrate for ABC1, while cells overexpressing ABC1 displayed a distinctive morphology, characterized by plasma membrane protrusions and resembling echinocytes that form when there are excess lipids in the outer membrane hemileaflet.
Journal ArticleDOI

ATP-binding Cassette Transporter A1 (ABCA1) Functions as a Cholesterol Efflux Regulatory Protein *

TL;DR: The data suggest that the binding of apoA-I to ABCA1 leads to the formation of phospholipid-apoA- I complexes, which subsequently promote cholesterol efflux in an autocrine or paracrine fashion.