The SREBP Pathway: Regulation of Cholesterol Metabolism by Proteolysis of a Membrane-Bound Transcription Factor
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This research was supported by grants from the National Institutes of Health (HL20948) and the Perot Family Foundation.About:
This article is published in Cell.The article was published on 1997-05-02 and is currently open access. It has received 3626 citations till now. The article focuses on the topics: Sterol response element binding.read more
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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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Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis
Robert A. Koeth,Zeneng Wang,Bruce S. Levison,Jennifer A. Buffa,Elin Org,Brendan Sheehy,Earl B. Britt,Xiaoming Fu,Yuping Wu,Lin Li,Jonathan D. Smith,Joseph A. DiDonato,Jun Chen,Hongzhe Li,Gary D. Wu,James D. Lewis,Manya Warrier,J. Mark Brown,Ronald M. Krauss,W.H. Wilson Tang,Frederic D. Bushman,Aldons J. Lusis,Stanley L. Hazen +22 more
TL;DR: It is demonstrated that metabolism by intestinal microbiota of dietary l-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice, and intestinal microbiota may contribute to the well-established link between high levels of red meat consumption and CVD risk.
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Peroxisome proliferator-activated receptors: nuclear control of metabolism.
Béatrice Desvergne,Walter Wahli +1 more
TL;DR: This work has shown that direct expression of PPAR mRNAs in the absence of a specific carrier gene results in down-regulation in the activity of other PPARs, and these properties are consistent with those of a “spatially aggregating substance”.
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Atherosclerosis: The Road Ahead
TL;DR: Elevated levels of serum cholesterol are probably unique through the hepatic LDL receptor pathway, as evi-in being sufficient to drive the development of athero-denced by the fact that lack of functional LDL receptors sclerosis in humans and experimental animals, even in is responsible for the massive accumulation of LDL in the absence of other known risk factors.
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Understanding Adipocyte Differentiation
TL;DR: Characterization of regulatory regions of adipose-specific genes has led to the identification of the transcription factors peroxisome proliferator-activated receptor-gamma and CCAAT/enhancer binding protein (C/EBP), which play a key role in the complex transcriptional cascade during adipocyte differentiation.
References
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The Metabolic and Molecular Bases of Inherited Disease
TL;DR: In this paper, the authors present a list of disorders of MITOCHONDRIAL FUNCTION, including the following: DISORDERS OF MIOCHONDRIC FERTILITY XIX, XVI, XIX.
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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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The ancient regulatory-protein family of WD-repeat proteins
TL;DR: WD proteins are made up of highly conserved repeating units usually ending with Trp-Asp (WD), and criteria for grouping such proteins into functional subfamilies are defined.
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Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice
Martin Citron,David Westaway,Weiming Xia,George A. Carlson,Thekla S. Diehl,G. Levesque,Kelly Johnson-Wood,Michael K. Lee,Peter Seubert,Angela Davis,Dora Kholodenko,Ruth Motter,R. Sherrington,Billie J. Perry,Hong Yao,Robert Strome,Ivan Lieberburg,Johanna M. Rommens,Soyeon Kim,Dale Schenk,Paul E. Fraser,Peter St. George Hyslop,Dennis J. Selkoe +22 more
TL;DR: The data demonstrate that the preseniiin mutations cause a dominant gain of function and may induce AD by enhancing Aβ42 production, thus promoting cerebral β-amyloidosis.