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- Table of Contents
Facts about Angiopoietin-related protein 3.
Has a stimulatory effect on plasma triglycerides (TG), which is accomplished by suppressing plasma TG clearance via inhibition of LPL activity. The inhibition of LPL activity seems to be an indirect mechanism involving recruitment of proprotein convertases PCSK6 and FURIN to LPL leading to cleavage and dissociation of LPL from the cell surface; the purpose doesn't require ANGPTL3 proteolytic cleavage but seems to be mediated by the N-terminal domain, and isn't inhibited by GPIHBP1 (PubMed:12097324, PubMed:19318355, PubMed:20581395).
Human | |
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Gene Name: | ANGPTL3 |
Uniprot: | Q9Y5C1 |
Entrez: | 27329 |
Belongs to: |
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No superfamily |
AGNPT5; Ang-5; angiopoietin 5; Angiopoietin-5; angiopoietin-like 3; Angiopoietin-like Protein 3; angiopoietin-related protein 3; ANGPT5angiopoietin-5; ANGPTL3; FHBL2
Mass (kDA):
53.637 kDA
Human | |
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Location: | 1p31.3 |
Sequence: | 1; NC_000001.11 (62597520..62606313) |
Expressed principally in liver. Weakly expressed in kidney. Binds to adipocytes. Increased expression and colocalization with activated ITGB3 in glomeruli of patients with nephrotic syndrome showing effaced podocyte foot processes (at protein level).
Secreted. Cell projection, lamellipodium. Colocalized with HSPG2 and activated ITGB3 on podocytes.
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Angiopoietin-like proteins (ANGPTL) are structurally similar to angiopoietins. These secreted proteins contain Coiled-coil domains on the N-terminus and fibrinogen-like regions on the C-terminus. The main difference between ANGPTL3 and Tie-2 is that it doesn't interact with Tie-2.
Antibodies for Angiopoietin are available from Boster Bio. Boster Bio develops ELISA kits with picogram-level sensitivity and research antibodies. The company's portfolio includes more than 12,000 validated antibodies for IHC as well as WB and Flow. Boster Bio antibodies are tested quantitatively against the quantities of recombinant protein. The antibodies are tested against 250 non-transfected and transfected cell lines.
Angiopoietin LPL3 is an important molecule in the development of vascular cells. It also regulates the expression of angptl3 inside cardiac muscle and adipose tissue. However, the role of ANGPTL3 within metabolic processes is unclear, and improved detection methods are needed to maximize the protein's potential for use.
Angiopoietin levels in circulation were associated with TG and insulin levels after an intervention for weight loss. The association was not strong and did last even after repeated tests. Despite this limited evidence that the connection between the circulating ANGPTL3 and plasma lipids isn't clear. AngPTL3 levels were found to be negatively connected with TG levels in European Caucasian patients. However, they showed a positive relationship with other lipids.
FDA approved by the FDA Evinacumab DGNB as an inhibitor of angiopoietin like 3 (ANGPTL3) to treat homozygous familial high cholesterol (HoFH). This drug is an reconjugated human monoclonal anti-angPTL3 antibody. It is an Regeneron Pharmaceuticals product and was recently approved in the United States to treat homozygous familial high cholesterol (HoFH). It also received a positive review from the European Union.
AngPTL3 is a Protein Coding gene that is associated with several diseases, including Hypobetalipoproteinemia, Familial, 2 and 1. It is involved in Plasma lipoprotein remodelling and assembly as well as NR1H2-mediated signals and growth factor activation. ANGPTL3 is an important counterpart to ANGPTL2.
The Phase 3 study of Evkeeza has proven that it is safe and effective for patients with the relapsed or refractory condition of large B-cell lymphoma (B-cell lymphoma). The risk of cardiovascular events was not evaluated in the clinical study. This drug was developed with Regeneron's VelocImmune technology. Evinacumab-dgnb binds to ANGPTL3, which is a protein that is involved in the regulation of circulating cholesterol.
C44-Fc, an anti-ANGPTL3 antibody, has been shown to bind to ANGPTL3 proteins with high affinity. Its affinity for the CCD fragment in mANGPTL3 is greater than the monomeric VHH C44–His6. This suggests that C44Fc could be a good candidate for patients with ANGPTL3 related disease.
Scientists initially developed a monoclonal antibody that captures the hANGPTL3Fc protein in order to create a humanized anti-hANGPTL3 antibody. They also created a C44–His6 monoclonal antibody with an HRP tag to detect the presence of hANGPTL3Fc antigen (S17-K170). After two hours at 25 degrees Celsius, C44-His6 could be added. The monoclonal antibody that resulted was detected by the His tag polyclonal antibody utilizing HRP (1:10,000 dilution).
While EVKEEZA is safe for women who are breastfeeding however, it is not recommended for pregnant women. It has been linked to serious hypersensitivity reactions, such as anaphylaxis. Breastfeeding mothers should utilize effective contraception throughout treatment and at least five months following the last dose. It is essential to discuss the risks and benefits with your physician before you begin EVKEEZA.
Angiopoietin-like protein (ANGPTL) are a family of proteins that regulate triglyceride availability and aid in the maintenance of energy balance. The mutations in the ANGPTL3 genes result in significantly lower plasma lipid levels, which may translate into lower risk of developing ischaemic heart disease. Certain people may have low levels these proteins due to obesity or diabetes type 2 or other genetic disorders.
Two genes encode the ANGPTL3 gene, ZNF259 & BUD13. ZNF259 is an zinc finger protein plays a vital role in cell expansion, signal transmission and metabolism of lipids. BUD13 is a member of the splicing and retention complex that regulates nuclear pre-mRNA retention. An ANGPTL3-related drug could be a target for combined hyperlipidemia. Two genetic variants acting trans-acting are associated with ANGPTL3, such as the rs4360730 variant.
The angPTL3 protein is a major regulator of hepatic storage of lipids, possibly impacting insulin resistance. One study revealed a connection with angPTL3 levels as well as the risk of non-alcoholic steatohepatitis. Therefore, angptl3 is an important element in metabolic syndrome and could be involved in the pathogenesis of non-alcoholic steatosis.
Another human study looked at the role of ANGPTL3 the metabolism of lipoproteins and lipids. It identified loci near the APOA4-APOA5-ZNF259-BUD13 gene cluster. This locus has been identified as a potential therapeutic target for dyslipidemia. Two polynucleotide sequences can be found close to the ANGPTL3 cluster.
In one study, researchers examined the ANGPTL3 gene on nearly 60,000 individuals. Researchers looked at plasma lipid levels and found a decrease in patients suffering from LOF the ANGPTL3 mutation. The result was a 39% lower risk of developing ischaemic cardiovascular disease. This result has significant implications for research into cardiovascular health as it highlights the importance to examine the ANGPTL3 marker.
It is not clear if it is possible to distinguish the different protein fragments and its post-translational modifications. It is difficult to determine whether the functional fraction of ANGPTL3 is present in circulation or is mostly bound to the endothelial surface of adipose tissues, cardiac muscle and skeletal muscles, where it may inhibit the lipolysis process mediated by LPL. Further research is needed to determine the exact role of ANGPTL3 for LPL regulation.
The confirmation of the ANGPTL3 variant gene in DM is a positive step towards the development of novel metabolic markers and blood pressure. The variant in ANGPTL3's gene was associated with blood pressure and circulating triglycerides. Many factors were taken into consideration in determining the relationship between the mRNA ANGPTL3 and these variables. These included age and sex level as well as total energy intake, drinking habits, and gender.
The Angptl3 protein is degraded by proprotein convertases into biologically active N-terminal and inactive C-terminal fragments. Two sandwich ELISA tests have been developed to measure the concentration of ANGPTL3 plasma. The Biovendor test uses commercially available antibodies or biotin-labeled ANGPTL3 rabbit polyclonal antigen to determine the level of the protein in the blood. The Biovendor test can detect both full-length ANGPTL3 and cleaved forms of the protein.
The ANGPTL3 gene has been linked with cholesterol profiles in genome-wide association studies. Familial combined hypolipidaemia (FCH) is a condition that affects compound heterozygotes as well as gene homozygotes. Loss-of-function mutations of ANGPTL3 result in lower levels of all classes of lipoproteins. E40K is another variant of the gene associated with lower levels of plasma TG.
The gene rs11207997 from ANGPTL3 is associated with lower circulating TG and levels of TC than CC carriers. This genotype effect may be mediated by dietary factors, which could have a moderating impact on circulating TG levels. The opposite effect was observed in the case of intakes of Q2 or Q4. This study is not conclusive the genetic linkage between DM and DM are conclusive.
The ANGPTL3 genes are a group of genes that play important roles in lipid metabolism. The ANGPTL3 gene is part of a family of genes that regulate the level of lipids. It inhibits lipoprotein lipase's activity. The ANGPTL3 genes has recently been identified as a promising treatment for cardiovascular disease. A low level of ANGPTL3 is associated with hypolipidemia, and a lower risk of CVD in Caucasians.
Research has shown that deletion of Angptl3 lowers serum TG and triglyceride levels in patients suffering from familial combined hypolipidemia. These results were consistent with previous studies that investigated the function and expression of ANGPTL3 in patients with familial mixed hypolipidemia. In addition the gene silencing of Angptl3 reduced apoB release and reduced LDL/VLDL levels in patients with familial apolipoproteinemia.
PMID: 10644446 by Conklin D., et al. Identification of a mammalian angiopoietin-related protein expressed specifically in liver.
PMID: 11877390 by Camenisch G., et al. ANGPTL3 stimulates endothelial cell adhesion and migration via integrin alpha vbeta 3 and induces blood vessel formation in vivo.