ArticleProceedings of the National Academy of Sciences of the United States of America1986
Molecular cloning of partial cDNAs for rabbit liver apolipoprotein B and the regulation of its mRNA levels by dietary cholesterol.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1986. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 38 citations in OpenAlex.
- Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and plasma lipoprotein concentrations by defined dietary fats. Comparison of trimyristin, tripalmitin, tristearin and triolein.The Biochemical journal · 1995Article
- Structure of rabbit butyrylcholinesterase gene deduced from genomic clones and from cDNA with introns.Cellular and molecular neurobiology · 1991Article
- Atherogenic diet increases cholesteryl ester transfer protein messenger RNA levels in rabbit liver.The Journal of clinical investigation · 1990Article
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4 authors.
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Abstract
Apolipoprotein B (apoB) is the major protein of plasma very low density lipoprotein (VLDL) and low density lipoprotein (LDL). Here we report the molecular cloning of cDNAs for rabbit liver apoB, by use of the expression vector lambda gt11, and the use of these cDNAs to study the regulation of apoB mRNA levels by dietary cholesterol. The beta-galactosidase-apoB fusion proteins expressed by recombinant clones were identified with guinea pig anti-rabbit LDL antibodies. The cloned cDNAs hybridized to an 18-kilobase mRNA that was present in liver and intestine. Slot blot analysis showed that this mRNA was not present in other tissues studied, with the possible exception of kidney. When rabbits are fed a high-cholesterol diet, they develop severe hypercholesterolemia. Most of the excess cholesterol is contained in beta-VLDL, a cholesteryl ester-rich lipoprotein that contains apoB and apoE. We addressed the question of whether increased apoB mRNA levels, and by inference increased apoB synthetic rates, are responsible for the accumulation of beta-VLDL. A comparison of apoB mRNA levels showed that cholesterol-fed rabbits had lower liver apoB mRNA levels than control rabbits. We suggest that the accumulation of plasma beta-VLDL in cholesterol-fed rabbits is not due to an increased production of beta-VLDL but solely due to a suppression of hepatic LDL receptors.
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