Active Recombinant Mouse Angptl3 Protein, His-tagged, Biotinylated
Cat.No. : | Angptl3-173M |
Product Overview : | Recombinant Mouse Angptl3(Ser17-Thr206) fused with His tag at C-terminal was expressed in CHO, Biotinylated. |
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- Gene Information
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Description : | Angiopoietin-like Protein 3 (ANGPTL3) is a secreted glycoprotein that is structurally related to the angiopoietins. Mature mouse ANGPTL3 contains an N-terminal coiled coil domain and a C-terminal fibrinogen-like domain. Mature mouse ANGPTL3 shares 77% aa sequence identity with human ANGPTL3. ANGPTL3 is expressed in the liver from early in development through adulthood. Full length ANGPTL3 circulates in the plasma as do the proteolytically separated N- and C-terminal fragments containing the coiled coil domain and fibrinogen-like domains, respectively. The cleavage of ANGPTL3 by Furin and Proprotein Convertase 5/6 is enhanced by its interaction with the related ANGPTL8. ANGPTL3 is found as 70 kDa, 50 kDa, and 32 kDa species and can form weakly associated noncovalent multimers in vitro. ANGPTL3 directly inhibits lipoprotein lipase (LPL) and endothelial lipase (EL), enzymes responsible for hydrolyzing circulating triglycerides and HDL phospholipids. This activity requires a putative heparin-binding motif which is N-terminal to the coiled coil domain. Proteolytic removal of the fibrinogen-like domain from the N-terminal fragment serves to activate ANGPTL3 and increase its ability to inhibit LPL in vitro and function in vivo [Ono 41804]. ANGPTL3 promotes an increase in circulating triglyceride levels without altering VLDL or HDL secretion or uptake. ANGPTL3 knockout mice are hypolipidemic and have elevated LPL activity. ANGPTL3 expression in vivo is upregulated by LXR agonists and downregulated by insulin, leptin, and agonists of TR beta or PPAR beta. Dysregulated ANGPTL3 expression and elevated plasma triglyceride levels are characteristic of some strains of obese and diabetic mice. ANGPTL3 does not bind Tie1 or Tie2, but its fibrinogen-like domain interacts with Integrin alpha V beta 3 to induce endothelial cell adhesion, migration, and neovascularization. ANGPTL3, secreted by fetal liver cells, also promotes the expansion of hematopoietic stem cells. |
Source : | CHO |
Species : | Mouse |
Tag : | His |
Predicted N Terminal : | Ser17 |
Form : | Lyophilized from a 0.2 μm filtered solution in MOPS, NaCl and CHAPS. |
Bio-activity : | Measured by its ability to promote the expansion of E16 rat liver mononuclear cells in vitro, in the presence of Recombinant Mouse SCF/c‑kit Ligand, Recombinant Mouse Thrombopoietin/Tpo, and Recombinant Mouse Flt‑3 Ligand. The ED50 for this effect is 20-120 ng/mL in the presence of a cross linking antibody, Mouse Anti-polyHistidine Monoclonal Antibody. |
Molecular Mass : | 23 kDa (unlabeled) |
Protein length : | Ser17-Thr206 |
Endotoxin : | <0.10 EU per 1 μg of the protein by the LAL method. |
Purity : | >95%, by SDS-PAGE with silver staining |
Notes : | Structure / Form: Biotinylated protein via sugars |
Storage : | Use a manual defrost freezer and avoid repeated freeze-thaw cycles. 12 months from date of receipt, -20 to -70 centigrade as supplied. 1 month, 2 to 8 centigrade under sterile conditions after reconstitution. 3 months, -20 to -70 centigrade under sterile conditions after reconstitution. |
Reconstitution : | Reconstitute at 100 μg/mL in PBS. |
Gene Name : | Angptl3 angiopoietin-like 3 [ Mus musculus ] |
Official Symbol : | Angptl3 |
Synonyms : | ANGPTL3; angiopoietin-like 3; angiopoietin-related protein 3; hypolipidemia; angiopoietin-like protein 3; hypl; |
Gene ID : | 30924 |
mRNA Refseq : | NM_013913 |
Protein Refseq : | NP_038941 |
UniProt ID : | Q9R182 |
Products Types
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◆ Lysates | ||
ANGPTL3-8862HCL | Recombinant Human ANGPTL3 293 Cell Lysate | +Inquiry |
Related Gene
For Research Use Only. Not intended for any clinical use. No products from Creative BioMart may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative BioMart.
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Q&As (27)
Ask a questionYes, research on ANGPTL3 is ongoing. Studies are being conducted to better understand its mechanisms of action, explore its potential therapeutic applications, and assess its long-term effects.
Yes, genetic testing for ANGPTL3 mutations can help identify individuals who may benefit from ANGPTL3-targeted therapies, although it is not currently a routine clinical practice and is typically reserved for research or specialized testing purposes.
The side effects of ANGPTL3-targeted therapies are still being investigated. However, some studies have reported mild side effects, such as injection site reactions, headache, and muscle pain. It is important to consult with a healthcare professional for more specific information on the potential side effects of ANGPTL3-targeted therapies.
Yes, ANGPTL3 deficiency is a relatively rare condition. It is usually caused by specific genetic mutations that impair ANGPTL3 production or function. The prevalence of ANGPTL3 deficiency in the general population is estimated to be very low.
Combination therapy with ANGPTL3 inhibitors and other cholesterol-lowering medications, such as statins, has shown potential for achieving more significant reductions in LDL cholesterol and triglyceride levels. However, the safety and efficacy of combining ANGPTL3 therapies with other medications may vary, and it is important to consult with a healthcare professional for personalized treatment recommendations.
ANGPTL3-targeted therapies have the potential to reduce the risk of cardiovascular disease by lowering LDL cholesterol and triglyceride levels. However, their exact role as a preventive measure is still being investigated, and more research is needed to determine their long-term efficacy and benefits in preventing heart disease.
Yes, clinical trials investigating ANGPTL3-targeted therapies have shown promising results in reducing LDL cholesterol and triglyceride levels in individuals with a genetic predisposition to high lipid levels.
Genetic variations in the ANGPTL3 gene may potentially affect an individual's response to lipid-lowering drugs. Certain variations may influence how an individual's body metabolizes and responds to these medications, leading to differences in their effectiveness. However, more research is needed to fully understand the impact of ANGPTL3 gene variations on drug response.
ANGPTL3 inhibitors, such as monoclonal antibodies or antisense oligonucleotides, are being explored as potential therapeutic approaches to reduce ANGPTL3 activity and lower lipid levels.
The potential interactions between ANGPTL3-targeted therapies and other cholesterol-lowering medications are still being studied. Combining these therapies with other medications may show additive or synergistic effects, but further research is needed to determine their compatibility and safety.
ANGPTL3-targeted therapies have the potential to lower LDL cholesterol and triglyceride levels, which are both risk factors for cardiovascular disease. By reducing ANGPTL3 activity, these therapies may help reduce the risk of heart disease and related complications.
ANGPTL3 has been associated with an increased risk of cardiovascular disease. Elevated levels of ANGPTL3 have been found to be a risk factor for atherosclerosis, coronary artery disease, and other cardiovascular events. Inhibiting ANGPTL3 activity has shown promise in reducing cardiovascular risk factors, such as LDL cholesterol and triglyceride levels.
There have been and continue to be clinical trials investigating ANGPTL3 therapies. These trials aim to evaluate the safety and efficacy of various drug candidates targeting ANGPTL3 in treating hyperlipidemia and related disorders.
Yes, there have been identified genetic mutations in the ANGPTL3 gene that can lead to significantly reduced or absent ANGPTL3 protein production. These mutations have been associated with lower levels of LDL cholesterol, triglycerides, and higher levels of high-density lipoprotein (HDL) cholesterol, resulting in the condition called familial hypobetalipoproteinemia.
While lifestyle changes alone may not directly impact ANGPTL3 levels, they can influence lipid and glucose metabolism, which in turn can affect ANGPTL3 regulation. Healthy lifestyle choices, including regular exercise, a balanced diet, weight management, and avoidance of smoking, can contribute to improved lipid and glucose metabolism, potentially leading to healthier ANGPTL3 levels.
Clinical trials have shown that ANGPTL3-targeted therapies have generally been well-tolerated, with few reported side effects. However, long-term safety data are still limited, and further research is needed to understand any potential side effects.
Yes, studies have shown that lifestyle factors such as diet and exercise can influence ANGPTL3 levels. A high-sugar diet and sedentary behavior have been associated with higher ANGPTL3 levels, while a healthy, balanced diet and regular physical activity may help normalize its levels.
ANGPTL3-targeted therapies may be particularly beneficial for individuals with genetically determined high cholesterol levels, such as those with familial hypercholesterolemia. They may also be helpful for individuals who do not respond well to or cannot tolerate traditional cholesterol-lowering medications. However, further research is needed to identify specific populations that may benefit the most from these therapies.
Yes, there are drug therapies being developed that target ANGPTL3. These therapeutic approaches aim to inhibit the activity of ANGPTL3 to reduce LDL cholesterol and triglyceride levels in individuals with hyperlipidemia or other related conditions.
No, ANGPTL3-targeted therapies are still under development and have not yet received regulatory approval for widespread use. Further research is needed to determine their long-term effectiveness and safety profile.
While there is no specific dietary or lifestyle change that can directly lower ANGPTL3 levels, adopting a healthy lifestyle can indirectly help maintain balanced lipid metabolism. Regular physical activity, a balanced diet rich in fruits, vegetables, and whole grains, and avoiding excessive consumption of added sugars and unhealthy fats can benefit overall heart health and lipid profile, including LDL cholesterol and triglyceride levels.
Yes, ANGPTL3 deficiency has been associated with certain health benefits. Individuals with genetic mutations causing low or absent ANGPTL3 production have been found to have reduced risk of cardiovascular disease, lower LDL cholesterol, lower triglycerides, and higher HDL cholesterol levels. However, further research is needed to fully understand the potential benefits and any potential side effects of ANGPTL3 deficiency.
ANGPTL3 has been found to have additional roles beyond lipid metabolism. It has been implicated in angiogenesis (the formation of new blood vessels) and in regulating glucose metabolism.
Elevated levels of ANGPTL3 can result in decreased LPL activity, leading to increased levels of triglycerides and LDL cholesterol in the bloodstream.
Yes, genetic mutations that cause ANGPTL3 deficiency or loss-of-function have been associated with lower levels of LDL cholesterol and triglycerides.
Yes, there are approved ANGPTL3-targeted therapies available. One example is evinacumab, which was approved by the U.S. Food and Drug Administration (FDA) in February 2021 for the treatment of homozygous familial hypercholesterolemia (HoFH), a rare genetic disorder characterized by extremely high cholesterol levels. Evinacumab is an antibody that targets and inhibits ANGPTL3, leading to decreased LDL cholesterol levels.
One limitation of ANGPTL3-targeted therapies is the high cost, as they are currently expensive medications. This can limit their accessibility and affordability for some individuals. Additionally, long-term safety data are still limited, and potential side effects or interactions with other medications need to be further explored.
Customer Reviews (5)
Write a reviewOne of the standout advantages offered by the manufacturer is their excellent technical support.
The ANGPTL3 protein is of exceptional quality, meeting all my experimental requirements with precision and reliability.
They continuously stay up-to-date with the latest scientific advancements and customer feedback, allowing them to refine the ANGPTL3 protein based on emerging trends.
This exceptional level of support enables me to overcome challenges efficiently and progress smoothly with my research.
They provide comprehensive assistance, ensuring that any queries or concerns I have regarding the ANGPTL3 protein are promptly addressed.
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