J
Joseph L. Goldstein
Researcher at University of Texas Southwestern Medical Center
Publications - 559
Citations - 155087
Joseph L. Goldstein is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: LDL receptor & Cholesterol. The author has an hindex of 207, co-authored 556 publications receiving 149527 citations. Previous affiliations of Joseph L. Goldstein include University of Texas System & University of Texas Health Science Center at San Antonio.
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Journal ArticleDOI
A receptor-mediated pathway for cholesterol homeostasis.
TL;DR: The approach was to apply the techniques of cell culture to unravel the postulated regulatory defect in FH, which led to the discovery of a cell surface receptor for a plasma cholesterol transport protein called low density lipoprotein (LDL) and to the elucidation of the mechanism by which this receptor mediates feedback control of cholesterol synthesis.
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Regulation of the mevalonate pathway.
TL;DR: The mevalonate pathway produces isoprenoids that are vital for diverse cellular functions, ranging from cholesterol synthesis to growth control, and could be useful in treating certain forms of cancer as well as heart disease.
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SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver
TL;DR: The complex, interdigitated roles of these three SREBPs have been dissected through the study of ten different lines of gene-manipulated mice and form the subject of this review.
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The SREBP Pathway: Regulation of Cholesterol Metabolism by Proteolysis of a Membrane-Bound Transcription Factor
TL;DR: This research was supported by grants from the National Institutes of Health (HL20948) and the Perot Family Foundation.
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Binding Site on Macrophages that Mediates Uptake and Degradation of Acetylated Low Density Lipoprotein, Producing Massive Cholesterol Deposition
TL;DR: It is hypothesized that this macrophage uptake mechanism may mediate the degradation of denatured LDL in the body and thus serve as a "backup" mechanism for the previously described receptor-mediated degradation of native LDL that occurs in parenchymal cells.