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Robert L. Hamilton

Researcher at University of California, San Francisco

Publications -  81
Citations -  9114

Robert L. Hamilton is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Very low-density lipoprotein & Apolipoprotein B. The author has an hindex of 51, co-authored 81 publications receiving 8930 citations. Previous affiliations of Robert L. Hamilton include University of Texas Southwestern Medical Center & Boston Children's Hospital.

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Discoidal bilayer structure of nascent high density lipoproteins from perfused rat liver.

TL;DR: Rat livers perfused without added plasma proteins suggest that the liver secretes disk-shaped lipid bilayer particles which represent both the nascent form of high density lipoproteins and preferred substrate for lecithin-cholesterol acyltransferase.
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Analysis of the role of microsomal triglyceride transfer protein in the liver of tissue-specific knockout mice

TL;DR: It is concluded that MTP is essential for transferring the bulk of triglycerides into the lumen of the ER for VLDL assembly and is required for the secretion of apo B-100 from the liver.
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Apoprotein composition of very low density lipoproteins of human serum.

TL;DR: In this paper, the tetramethylurea was used to delipidates the lipoprotein and selectively precipitates apolipoprotein B. The mean content of apoprotein B in 43 samples from normolipidemic and hyperlipemic subjects was 36.9(+/-1.2 SEM)% of total protein, the distribution of the major soluble apoproteins as mean (+/-SEM) percentage of the soluble fraction was : R-serine, 5.3+/-o.5; arginine-rich, 20.
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Resistance to diet-induced hypercholesterolemia and gallstone formation in ACAT2-deficient mice.

TL;DR: The results indicate that ACAT2 has an important role in the response to dietary cholesterol, and suggest that ACat2 inhibition may be a useful strategy for treating hypercholesterolemia or cholesterol gallstones.
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Subcellular localization of B apoprotein of plasma lipoproteins in rat liver.

TL;DR: Evidence suggests a sequence for the biosynthesis of VLDL that differs in some respects from that proposed by others: (a) the triglyceride-rich particle originates in smooth ER where triglycerides are synthesized; (b) at the junction of the smooth and rough ER the particle receives apoproteins synthesized in the rough ER.