Active Recombinant Human ANGPT1 Protein, His-tagged, Biotinylated
|Product Overview :||Recombinant Human ANGPT1(Ser20-Phe498) fused with His tag at C-terminal was expressed in NS0, Biotinylated.|
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|Description :||Angiopoietin-1 (Ang-1) is a secreted glycoprotein that plays a critical role in the development and maintenance of the vascular system. It contains a N-terminal coiled-coil region and a C-terminal fibrinogen-like domain separated by a short flexible region. Mature human Angiopoietin-1 shares 97% amino acid sequence identity with mouse and rat Angiopoietin-1. It is expressed by vascular smooth muscle cells and pericytes as an approximately 70 kDa molecule that associates into disulfide-linked homotrimers, tetramers, and pentamers. Angiopoietin-1 binds and activates the receptor tyrosine kinase Tie-2, and its association into tetramers is important for full Tie-2 activation. Angiopoietin-1 ligation of Tie-2 on vascular endothelial cells (EC) induces the development and branching of blood vessels. In sub-confluent EC (i.e. during angiogenesis), Angiopoietin-1 promotes EC motility and Tie-2 localization at the trailing edge of the cell. In confluent EC (i.e. in homeostasis), multimeric Angiopoietin-1 enhances vascular integrity by promoting the in trans homotypic association of Tie-2 between EC or with the substratum. In addition, Angiopoietin-1 suppresses several VEGF-induced effects on the vasculature including endothelial permeability, stretch-induced release of Angiopoietin-2, and up-regulation of the leukocyte adhesion molecules VCAM-1, ICAM-1, and E-Selectin. Angiopoietin-1 also interacts with a variety of integrins and the extracellular matrix independently of Tie-2. These interactions support the adhesion, migration and stress resistance of EC, fibroblasts, and myocytes. Angiopoietin-1 can protect against pulmonary arterial hypertension, reduce the extent of fibrosis and remodeling in infarcted diabetic myocardium, and enhance tumor progression and metastasis.|
|Source :||Mammalian cells|
|Predicted N Terminal :||Ser20|
|Form :||Lyophilized from a 0.2 μm filtered solution in Tris-Citrate and NaCl with BSA as a carrier protein.|
|Bio-activity :||Measured by its ability to inhibit serum deprivation induced apoptosis in HUVEC human umbilical vein endothelial cells. Kwak, H.J. et al. (1999) FEBS Letters 448:249. The ED50 for this effect is 10-40 ng/mL in the presence of 5 μg/mL of a cross-linking an|
|Molecular Mass :||56 kDa (unlabeled)|
|Protein length :||Ser20-Phe498|
|Endotoxin :||<1.0 EU per 1 μg of the protein by the LAL method.|
|Purity :||>90%, by SDS-PAGE with silver staining|
|Notes :||Structure / Form: Oligomer|
|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
|Reconstitution :||Reconstitute at 10 μg/mL in PBS containing at least 0.1% human or bovine serum albumin.|
|Gene Name :||ANGPT1 angiopoietin 1 [ Homo sapiens ]|
|Official Symbol :||ANGPT1|
|Synonyms :||ANGPT1; angiopoietin 1; angiopoietin-1; Ang1; KIAA0003; ANG-1; AGP1; AGPT; ANG1;|
|Gene ID :||284|
|mRNA Refseq :||NM_001146|
|Protein Refseq :||NP_001137|
|UniProt ID :||Q15389|
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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.
Q&As (18)Ask a question
While ANGPT1 is primarily associated with blood vessel formation and stability, recent studies have indicated potential involvement of ANGPT1 in neurological disorders. For example, it has been suggested that ANGPT1 may play a role in Alzheimer's disease, stroke, and neuroinflammation. However, further research is required to understand the precise role of ANGPT1 in these neurological conditions.
The activity of ANGPT1 is tightly regulated by different factors. Vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-beta) are known to collaborate with ANGPT1 to regulate blood vessel formation and stability. Several transcription factors, signaling molecules, and microRNAs have also been identified as regulators of ANGPT1 expression.
Yes, ANGPT1 is involved in vascular development during embryogenesis. It promotes blood vessel maturation and stabilization, which is essential for the formation of a functional vascular system. ANGPT1, along with its receptor Tie2, regulates the interactions between endothelial cells and pericytes, leading to the formation of stable blood vessels. Deficiency in ANGPT1 or Tie2 during embryonic development can result in abnormal blood vessel formation and defects in vascular morphogenesis.
ANGPT1 has been implicated in tumor angiogenesis, which is the process of formation of new blood vessels to supply oxygen and nutrients to tumors. Its expression is often elevated in certain types of cancer, and it promotes tumor growth and metastasis. Therefore, ANGPT1 has been considered as a potential therapeutic target for cancer. Several approaches, such as blocking ANGPT1/Tie2 signaling using antibodies or small molecules, have shown promising results in preclinical studies. However, further research is needed to determine the efficacy and safety of ANGPT1-based therapies in clinical settings.
Several factors have been identified that can either inhibit or activate ANGPT1 signaling. For example, VEGF, another pro-angiogenic factor, can promote ANGPT1 expression and enhance its activity. On the other hand, certain molecules, such as angiostatin and endostatin, have been shown to block ANGPT1-induced angiogenesis. Furthermore, there are ongoing studies to develop therapeutics that directly target ANGPT1 or its receptor Tie2 to modulate its activity.
Yes, ANGPT1 is involved in the process of wound healing. It promotes angiogenesis in the injured area, which helps to supply oxygen and nutrients to the healing tissues. ANGPT1 also plays a role in tissue remodeling and repair by promoting the migration of certain cells, such as fibroblasts, which contribute to wound closure. Additionally, it may help to reduce inflammation and support the formation of new blood vessels during the healing process.
While there are currently no registered clinical trials specifically investigating ANGPT1 as a therapeutic target, there are ongoing studies exploring the efficacy of agents that block or modulate ANGPT1 signaling in various diseases, including cancer. These studies aim to evaluate the safety and effectiveness of ANGPT1-targeted therapies in preclinical and clinical settings and may provide valuable insights into the potential clinical applications of ANGPT1 inhibition or stimulation.
Yes, ANGPT1 has been implicated in wound healing and tissue repair processes. It promotes angiogenesis and stabilizes newly formed blood vessels, which are crucial for delivering oxygen and nutrients to healing tissues. ANGPT1 also stimulates the recruitment and maturation of pericytes, which aid in wound healing by providing structural support to blood vessels.
While ANGPT1's primary role is in angiogenesis, the formation of blood vessels, it has also been reported to play a role in lymphangiogenesis, the formation of lymphatic vessels. ANGPT1-Tie2 signaling has been shown to regulate lymphatic vessel growth and maturation. However, the precise mechanisms and significance of ANGPT1 in lymphangiogenesis are still under investigation.
Currently, no inherited disorders directly linked to ANGPT1 gene mutations have been reported. However, dysregulation of ANGPT1 expression and abnormal Tie2 signaling have been implicated in various diseases, including retinopathy, inflammatory conditions, and cancer.
At present, there are no clinical trials specifically focused on ANGPT1-based therapies. However, there are clinical trials investigating the use of ANGPT1 in combination with other molecules, such as VEGF inhibitors or immune checkpoint inhibitors, for various cancers. These trials aim to assess the efficacy and safety of ANGPT1-targeted therapies as part of a comprehensive treatment strategy.
While genetic mutations or polymorphisms in the ANGPT1 gene have not been extensively studied, some studies have reported associations with certain diseases. For example, specific variations in the ANGPT1 gene have been linked to susceptibility to age-related macular degeneration (AMD) and diabetic retinopathy. However, more research is needed to establish the significance of these genetic variants and their impact on disease development.
ANGPT1 is not commonly used as a diagnostic marker for specific diseases. However, its levels have been found to be altered in certain conditions, such as cardiovascular diseases, diabetic retinopathy, and sepsis, which suggests its potential as a biomarker. Further research is needed to establish ANGPT1 as a reliable diagnostic marker.
The transcriptional regulation of ANGPT1 is complex and involves various factors. Several transcription factors, such as hypoxia-inducible factors (HIF-1α), Sp1, and NF-κB, have been shown to directly bind to the ANGPT1 gene promoter and regulate its expression. In addition, signaling pathways like VEGF and TGF-beta can influence ANGPT1 expression by activating downstream transcription factors that interact with the ANGPT1 promoter region. MicroRNAs also play a role in post-transcriptional regulation of ANGPT1 expression.
ANGPT1 has shown potential therapeutic value in various medical conditions. It is being explored for its ability to promote blood vessel formation and stabilize existing blood vessels in disorders such as cardiovascular diseases, diabetic retinopathy, and tumor angiogenesis. Additionally, ANGPT1 has been investigated for its potential in tissue engineering and regenerative medicine approaches.
One potential concern with targeting ANGPT1 for therapy is the potential for adverse effects on normal physiological processes. ANGPT1 plays a crucial role in vascular development and stability, and its blockade or manipulation could have unforeseen consequences on blood vessel formation and function. Additionally, since ANGPT1 is involved in various biological processes, there might be off-target effects that could lead to unintended consequences. Therefore, careful evaluation of ANGPT1-targeted therapies is necessary to ensure safety and minimize potential side effects.
ANGPT1 can have both tumor-suppressive and tumor-promoting effects depending on the context. In some cancers, ANGPT1/Tie2 signaling can inhibit tumor angiogenesis and limit metastasis. Conversely, in certain types of tumors, ANGPT1 can induce angiogenesis, promoting tumor growth and metastasis. Further research is necessary to understand the complexities of ANGPT1's role in different types and stages of cancer.
Several molecules have been identified as modulators of ANGPT1/Tie2 signaling. For example, antibodies that activate or block Tie2 receptor have been developed for experimental purposes. In addition, small-molecule inhibitors targeting the ANGPT1/Tie2 pathway are being investigated as potential therapeutic agents for diseases involving abnormal angiogenesis.
Customer Reviews (5)Write a review
ANGPT1 protein's utility extends to protein electron microscopy structure analysis, where it plays a crucial role in investigating the detailed architecture and conformational changes of proteins. -
It exhibits exceptional performance in ELISA assays, making it an excellent choice for researchers studying angiopoietins, angiogenesis, or vascular biology. -
It demonstrates excellent performance in ELISA assays, making it an ideal choice for researchers studying protein-protein interactions, antibody detection, or biomarker identification. -
ANGPT1 protein is highly recommended for use in various research applications, including ELISA and protein electron microscopy structure analysis. -
ANGPT1 protein's remarkable performance in ELISA and protein electron microscopy structure analysis positions it as a valuable tool in various fields, including cardiovascular research, developmental biology, and molecular medicine. -
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