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Friedhelm Schroeder

Researcher at Texas A&M University

Publications -  313
Citations -  15215

Friedhelm Schroeder is an academic researcher from Texas A&M University. The author has contributed to research in topics: Fatty acid-binding protein & Fatty acid. The author has an hindex of 66, co-authored 313 publications receiving 14666 citations. Previous affiliations of Friedhelm Schroeder include United States Department of Veterans Affairs & University of Cincinnati.

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Cellular uptake and intracellular trafficking of long chain fatty acids.

TL;DR: The emerging picture is that the cell has multiple, overlapping mechanisms that assure adequate uptake and directed intracellular movement of LCFA required for maintenance of physiological functions.
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Membrane cholesterol dynamics: cholesterol domains and kinetic pools.

TL;DR: This work examines the role of high-density lipoprotein, cholesterol lowering drugs, and intracellular lipid transfer proteins in membrane sterol domain structure and sterol movement between membranes to elucidation of cholesterol dynamics in membranes.
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Gene structure, intracellular localization, and functional roles of sterol carrier protein-2.

TL;DR: Although the 13 kDa SCP-2 is the most studied of these proteins, because it exhibits diversity of its ligand partners, new potential physiological function(s) are still being proposed and questions regarding potential compensation by other proteins with overlapping specificity are only beginning to be resolved.
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Role of Fatty Acid Binding Proteins and Long Chain Fatty Acids in Modulating Nuclear Receptors and Gene Transcription

TL;DR: The hypothesis that cytoplasmic lipid binding proteins transfer and channel lipidic ligands into nuclei for initiating nuclear receptor transcriptional activity to provide new lipid nutrient signaling pathways that affect lipid and glucose catabolism and storage is proposed.
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Liver fatty acid-binding protein and obesity

TL;DR: Data suggest that L-FABP could have an important role in preventing age- or diet-induced obesity and in reducing hepatic LCFA uptake/oxidation and increasing LCFAs available for oxidation in muscle and/or storage in adipose.