ANGPTL3
- Known as:
- ANGPTL3
- Catalog number:
- CYT-248
- Product Quantity:
- 2µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- ANGPTL3
Related genes to: ANGPTL3
- Gene:
- ANGPTL3 NIH gene
- Name:
- angiopoietin like 3
- Previous symbol:
- ANGPT5
- Synonyms:
- -
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-07
- Date modifiied:
- 2015-11-11
Related products to: ANGPTL3
Related articles to: ANGPTL3
- Angiopoietin-like 8 (ANGPTL8) is a calorically responsive regulator of lipoprotein lipase (LPL). It does this by forming complexes with ANGPTL3 or ANGPTL4 that either inhibit LPL in oxidative tissues or preserve LPL activity in adipose tissue, respectively. Human heterozygous (reference allele/alternate allele, R/A) carriers of rs145464906/p.Q121X and rs760351239/p.Q131X ANGPTL8 protein truncating variants (PTVs) have favorable lipid profiles and decreased cardiovascular risk. Given the purported role of ANGPTL8 in redirecting circulating lipids in response to feeding, it is not clear why these PTVs should profile as they do. We elucidated this process by investigating these ANGPTL8 PTVs along with several novel ANGPTL8 putative loss of function (pLOF) variants, including a splice donor variant rs774984872/c.459 + 1G > T that was predicted to result in an ANGPTL8 truncation (p.K165X), in a consanguineous population from the Pakistan Genomic Resource (PGR). We observed lower TG, lower total cholesterol, and increased HDL-C in heterozygous carriers of these variants, consistent with previous reports for p.Q121X and p.Q131X and confirmed decreased ANGPTL3/8 and ANGPTL4/8 complex levels in serum samples from these carriers compared to non-carriers (R/R). Biochemically, the p.Q121X, p.Q131X and c.459 + 1G > T mutations showed dramatically reduced ANGPTL3/8 complex-mediated LPL inhibition while only modestly decreasing ANGPTL4/8-mediated preservation of LPL activity. Furthermore, a cohort of 14 participants that included 8 non-carriers, 5 heterozygous carriers and a single homozygous (A/A) individual of the c.459 + 1G > T pLOF variant were recruited for kinetic studies following standard mixed meal tolerance tests. Heterozygous carriers showed significantly reduced postprandial TG excursions compared to non-carriers. Together, these results support the concept that pLOF variants in ANGPTL8 result in favorable lipid profiles by selectively reducing ANGPTL3/8-mediated LPL inhibition while largely maintaining ANGPTL4/8-mediated preservation of LPL activity. - Source: PubMed
Publication date: 2026/04/29
Abadi ArkanChen Yan QKhalid ShareefWilliams KyliaZhen Eugene YLi HongxiaSiegel RobertHartley MaryaliceBeyer Thomas PatrickDeBowles DanishaQian Yue-WeiRahseed AsifKhan Maleeha ZamanJahanzaib MuhammadMian Muhammad RehanSultana RiffatJalal AnjumAbbas ShahidMuddassir AmbreenMohsin Saima NazMukhtar ShahidMahmood AdilRyan Timothy PMichael Laura FRuotolo GiacomoSaleheen DanishWen YiKonrad Robert JBhatnagar Pallav - Fenofibrate and other fibrates are peroxisome proliferator-activated receptor alpha (PPARα) agonists that are used to lower plasma triglyceride (TG) levels. Although fibrates are effective in decreasing TG, their ability to reduce adverse cardiovascular events and cardiovascular mortality in clinical trials has been disappointing. PPARα agonists influence the expression of dozens of genes, but the mechanisms by which they lower TG levels are incompletely understood. Apolipoprotein A5 (APOA5) and angiopoietin-like proteins 3, 4, and 8 (ANGPTL3/4/8) are important regulators of intravascular TG metabolism. To explore if their regulation might explain the TG-lowering effect of fibrates, we examined the impact of fenofibrate on the expression of APOA5 and the ANGPTL3/4/8 proteins in mice and humans. In wild-type mice, fenofibrate reduced plasma TG levels, increased Angptl4 and Angptl3 transcripts in the liver, and reduced Angptl8 and Apoa5 transcripts. Fenofibrate also decreased plasma APOA5 levels and increased levels of ANGPTL3, ANGPTL3/8, ANGPTL4/8, and the C-terminal domain of ANGPTL4 (CD-ANGPTL4). These changes would be predicted to increase rather than decrease TG levels. The TG reduction by fenofibrate was maintained in Apoa5-deficient mice, further indicating that APOA5 is not involved in TG lowering by fenofibrate. In humans, fenofibrate reduced TG without increasing APOA5 levels or reducing ANGPTL3/8 levels. In addition, fenofibrate treatment increased levels of ANGPTL3, ANGPTL4/8, and CD-ANGPTL4. The collective human and mouse data suggest that APOA5 and ANGPTL3/4/8 proteins do not mediate fenofibrate-induced TG lowering. Our findings are noteworthy because elevated levels of ANGPTL3, ANGPTL4/8, and CD-ANGPTL4 are associated with increased cardiovascular mortality. - Source: PubMed
Publication date: 2026/04/27
Yang YeSmith SydneyChen Yan QLi HongxiaZhen Eugene YSloan John HSiegel Robert WQian YueweiWen YiJung HyesooScheithauer Julia LKersten SanderYoung Stephen GKonrad Robert J - Inhibition of angiopoietin-like protein 3 (ANGPTL3) has been proposed as a promising approach to reduce residual cardiovascular risk. We conducted a meta-analysis of randomized controlled trials (RCTs) to provide a comprehensive evaluation of the metabolic effects of ANGPTL3 inhibitors. - Source: PubMed
Publication date: 2026/04/22
Xie SiningGalimberti FedericaOlmastroni ElenaCatapano Alberico LCasula Manuela - Concomitant liver and kidney injury is a critical pathological feature of metabolic disorders, but current organ-specific therapies often fail to provide cross-protection. Lipotoxicity is a core mechanism linking damage in both organs. Therefore, this study aimed to investigate whether simultaneously targeting ANGPTL3 and IL-1β could attenuate lipotoxicity and thereby ameliorate concomitant liver and kidney injury. - Source: PubMed
Publication date: 2026/04/17
Xu ShuwenWang LongfeiDou ZihanHu XiaozhiCao ZhonglianZhang YuanzhenJiang XianhanWu TaoLi ZhuojinNan YanyangZhu AnBai YuZou ZiqianZhang XuyaoZeng XianHe HaidongWang ShaofeiJu DianwenFan Jiajun - Prostate cancer (PCa) cells are known to heavily depend on lipids to support their growth. We hypothesized that hyperlipidemic factors, for which inhibitors are already available and used to treat cardiovascular disease, would be dysregulated in metastatic PCa (mPCa). The goal of this case-control study, including 35 men per group, was to compare the levels of PCSK9, ANGPTL3, Apo CIII, leptin, and the lipid profile in patients with mPCa versus localized Gleason 8/9 PCa (lPCa) and patients at risk of developing PCa (controls). - Source: PubMed
Publication date: 2026/04/07
Boulay GabrielKhodr MarwanBergeron Ann-CharlotteWong Chong ÉmilieJoncas France-HélèneCastonguay ChloéRobitaille KarineHovington HélèneFradet VincentBergeron AlainPouliot FrédéricBlais JonatanSeidah Nabil GCalon FrédéricGangloff Anne