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Angiopoietin-like 3

ANGPTL3, angiopoietin-like 3
The protein encoded by this gene is a member of the angiopoietin-like family of secreted factors. It is predominantly expressed in the liver, and has the characteristic structure of angiopoietins, consisting of a signal peptide, N-terminal coiled-coil domain and the C-terminal fibrinogen (FBN)-like domain. The FBN-like domain in angiopoietin-like 3 protein was shown to bind alpha-5/beta-3 integrins, and this binding induced endothelial cell adhesion and migration. This protein may also play a role in the regulation of angiogenesis. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Angpt1, HDL, Lipoprotein Lipase, ANGPTL4, HAD
Papers on ANGPTL3
The role of ANGPTL3 in controlling lipoprotein metabolism.
Jauhiainen et al., Helsinki, Finland. In Endocrine, Feb 2016
UNASSIGNED: Angiopoietin-like protein 3 (ANGPTL3) is a secretory protein regulating plasma lipid levels via affecting lipoprotein lipase- and endothelial lipase-mediated hydrolysis of triglycerides and phospholipids.
Gene-based therapies in lipidology: current status and future challenges.
Brisson et al., Montréal, Canada. In Curr Opin Lipidol, Dec 2015
Most advanced antisense oligonucleotide drugs target apolipoprotein C-III, apolipoprotein (a), angiopoietin-like 3, and diacylglycerol o-acyltransferase-2.
Circulating angiopoietin-like protein 8 (ANGPTL8) and ANGPTL3 concentrations in relation to anthropometric and metabolic profiles in Korean children: a prospective cohort study.
Choi et al., Seoul, South Korea. In Cardiovasc Diabetol, Dec 2015
BACKGROUND: Previous studies have shown that angiopoietin-like protein 8 (ANGPTL8), also called as betatrophin, acts together with ANGPTL3 to regulate lipid metabolism, glucose metabolism, and energy homeostasis.
Clinical significance of angiopoietin-like protein 3 expression in patients with glioblastoma.
Yan et al., In Neoplasma, Dec 2015
Angiopoietin-like protein 3 (ANGPTL3) is proven to be involved in angiogenesis and tumor development.
Update on the molecular biology of dyslipidemias.
Ramasamy, Worcester, United Kingdom. In Clin Chim Acta, Dec 2015
Mutations in the genes APOB, and ANGPTL3 and ANGPTL4 (that encode angiopoietin-like proteins which inhibit lipoprotein lipase activity) can further cause low levels of apoB containing lipoproteins.
Acute alcohol consumption downregulates lipoprotein lipase activity in vivo.
Kovář et al., Praha, Czech Republic. In Metabolism, Nov 2015
Therefore, we have studied the effects of acute moderate alcohol consumption on LPL activity and on the concentrations of angiopoietin-like proteins 3 and 4 (ANGPTL3 and ANGPTL4), which are known to inhibit LPL.
Insights from human congenital disorders of intestinal lipid metabolism.
Levy, Montréal, Canada. In J Lipid Res, May 2015
The influence of newly discovered proteins (proprotein convertase subtilisin/kexin type 9 and angiopoietin-like 3 protein) on fat absorption has also been provided.
Angiopoietin-like protein 3 is an indicator of prognosis in esophageal cancer patients.
Yu et al., Taizhou, China. In Int J Clin Exp Med, 2014
Angiopoietin-like protein 3 (ANGPTL3) plays an important role in angiogenesis.
Angiopoietin-like proteins 3, 4 and 8: regulating lipid metabolism and providing new hope for metabolic syndrome.
Teng et al., Harbin, China. In J Drug Target, 2014
ANGPTL3 plays a vital role in the regulation of the plasma levels of triglyceride and cholesterol, mainly via reversible inhibition of the lipoprotein lipase activity.
Genes associated with low serum high-density lipoprotein cholesterol.
Azizi et al., Tehrān, Iran. In Arch Iran Med, 2014
Genetic defects in ATP binding cassette protein (ABCA1), apolipoprotein (APO) A1, lecithin cholesteryl acyl transferase, Lipoprotein lipase (LPL), and angiopoietin-like 3 proteins (ANGPTL3) associated with low HDL-C.
Mutations in the ANGPTL3 gene and familial combined hypolipidemia: a clinical and biochemical characterization.
Arca et al., Roma, Italy. In J Clin Endocrinol Metab, 2012
Familial combined hypolipidemia segregates as a recessive trait so that apolipoprotein B- and apolipoprotein A-I-containing lipoproteins are comprehensively affected only by the total deficiency of Angptl3.
Identification of a novel mutation in the ANGPTL3 gene in two families diagnosed of familial hypobetalipoproteinemia without APOB mutation.
Blanco-Vaca et al., Barcelona, Spain. In Clin Chim Acta, 2012
It denominated familial combined hypolipidemia, which consist of a biochemical phenotype of low LDLc, low apoB, low TG and, unlike APOB mutations, low HDL cholesterol, due to a loss-of-function mutation in ANGPTL3.
Prevalence of ANGPTL3 and APOB gene mutations in subjects with combined hypolipidemia.
Averna et al., Palermo, Italy. In Arterioscler Thromb Vasc Biol, 2012
In a cohort of subjects with severe primary hypobetalipoproteinemia the prevalence of ANGPTL3 gene mutations responsible for a combined hypolipidemia phenotype is about 10%.
Characterization of three kindreds with familial combined hypolipidemia caused by loss-of-function mutations of ANGPTL3.
Bertolini et al., Genova, Italy. In Circ Cardiovasc Genet, 2012
the homozygous or compound heterozygous for ANGPTL3 loss-of-function mutations (p.G400VfsX5, p.I19LfsX22/p.N147X) had low plasma ANGPTL3 and moderately reduced low-density lipoprotein cholesterol but normal plasma high-density lipoprotein cholesterol.
Genetic variation in APOB, PCSK9, and ANGPTL3 in carriers of pathogenic autosomal dominant hypercholesterolemic mutations with unexpected low LDL-Cl Levels.
Fouchier et al., Amsterdam, Netherlands. In Hum Mutat, 2012
The prevalence and effect of mutations in ANGPTL3, in carriers of pathogenic autosomal dominant hypercholesterolemia mutations with unexpected low LDL-C levels.
Exome sequencing, ANGPTL3 mutations, and familial combined hypolipidemia.
Kathiresan et al., Boston, United States. In N Engl J Med, 2011
Found two distinct nonsense mutations in ANGPTL3 in 2 family members out of 38 with combined hypolipidemia.
Newly identified loci that influence lipid concentrations and risk of coronary artery disease.
Abecasis et al., Ann Arbor, United States. In Nat Genet, 2008
Overall, we identify strongly associated variants in eleven loci previously implicated in lipid metabolism (ABCA1, the APOA5-APOA4-APOC3-APOA1 and APOE-APOC clusters, APOB, CETP, GCKR, LDLR, LPL, LIPC, LIPG and PCSK9) and also in several newly identified loci (near MVK-MMAB and GALNT2, with variants primarily associated with high-density lipoprotein (HDL) cholesterol; near SORT1, with variants primarily associated with low-density lipoprotein (LDL) cholesterol; near TRIB1, MLXIPL and ANGPTL3, with variants primarily associated with triglycerides; and a locus encompassing several genes near NCAN, with variants strongly associated with both triglycerides and LDL cholesterol).
Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans.
Orho-Melander et al., Boston, United States. In Nat Genet, 2008
Of the six newly identified chromosomal regions, two were associated with LDL cholesterol (1p13 near CELSR2, PSRC1 and SORT1 and 19p13 near CILP2 and PBX4), one with HDL cholesterol (1q42 in GALNT2) and five with triglycerides (7q11 near TBL2 and MLXIPL, 8q24 near TRIB1, 1q42 in GALNT2, 19p13 near CILP2 and PBX4 and 1p31 near ANGPTL3).
Hepatic proprotein convertases modulate HDL metabolism.
Rader et al., Philadelphia, United States. In Cell Metab, 2007
Hepatic PCs reduce EL function through direct inactivating cleavage of EL as well as through activating cleavage of angiopoietin-like protein 3 (ANGPTL3), an endogenous inhibitor of EL.
Angiopoietin-like proteins stimulate ex vivo expansion of hematopoietic stem cells.
Lodish et al., Cambridge, United States. In Nat Med, 2006
Here we show, using microarray studies, that the HSC-supportive mouse fetal liver CD3(+) cells specifically express the proteins angiopoietin-like 2 (Angptl2) and angiopoietin-like 3 (Angptl3).
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