GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 08 Dec 2016.
Apolipoprotein C-III, apoC-III, APOC3
Apolipoprotein C-III is a very low density lipoprotein (VLDL) protein. APOC3 inhibits lipoprotein lipase and hepatic lipase; it is thought to delay catabolism of triglyceride-rich particles. The APOA1, APOC3 and APOA4 genes are closely linked in both rat and human genomes. The A-I and A-IV genes are transcribed from the same strand, while the A-1 and C-III genes are convergently transcribed. An increase in apoC-III levels induces the development of hypertriglyceridemia. [provided by RefSeq, Jul 2008] (from
Nobécourt et al., France. In J Lipid Res, Feb 2016
UNASSIGNED: A multiplexed assay was developed by mass spectrometry to analyze in a single run six major human apolipoproteins (Apos) involved in lipoprotein metabolism: ApoAI, ApoAII, ApoB100, ApoCII, ApoCIII, and ApoE.
Jankowski et al., Gdańsk, Poland. In Chem Phys Lipids, Feb 2016
UNASSIGNED: Lipoprotein lipase (LPL)-mediated triacylglycerol (TAG) hydrolysis in very low density lipoprotein (VLDL) is accompanied by the release of surface material containing phospholipids (PL), free cholesterol (FC) and apolipoproteins, E (apoE) and Cs (apoCII, apoCIII).
Orho-Melander, Malmö, Sweden. In J Intern Med, Nov 2015
Furthermore, identification of rare loss-of-function variants in genes such as PCSK9, NPC1L1, APOC3 and APOA5, which cause a markedly decreased risk of CHD and no adverse side effects, illustrates the power of translating genetic findings into novel mechanistic information and provides some optimism for the future of developing novel drugs, given the many genes associated with CHD in GWASs.
Boerwinkle et al., Houston, United States. In Nat Genet, Jun 2015
To test this hypothesis, we sequenced the exomes of 8,554 individuals and analyzed the effects of predicted LOF variants on 20 chronic disease risk factor phenotypes. Analysis of this sample as discovery and replication strata of equal size verified two relationships in well-studied genes (PCSK9 and APOC3) and identified eight new loci.
Gursky et al., Boston, United States. In Adv Exp Med Biol, 2014
Surprisingly, the rank order of the amino acid sequence propensity to form amyloid (apoB>apoA-II>apoC-II≥apoA-I, apoC-III, SAA, apoC-I>apoA-IV, apoA-V, apoE) does not correlate with the proteins' involvement in amyloidosis.