ALK-1 Protein, Cynomolgus (HEK293, His)
Based on 1 Customer Validation
ALK-1, also known as ACVRL1, is a type I receptor for TGF-β superfamily with 2 ligands, BMP9 and BMP10. ALK-1 is predominantly expressed in endothelial cells and plays a critical role in regulating developmental and pathological angiogenesis. ALK-1 Protein, Cynomolgus (HEK293, His) is produced in HEK293 cells with a C-Terminal His-tag. It consists of 118 amino acids (D22-Q118).
- Species: Cynomolgus
- Source: HEK293
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Storage:Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.
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Biological Activity
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Technical Parameters
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Product Properties
- Documentation
- References
- Help & FAQs
Biological Activity
Description
ALK-1, also known as ACVRL1, is a type I receptor for TGF-β superfamily with 2 ligands, BMP9 and BMP10. ALK-1 is predominantly expressed in endothelial cells and plays a critical role in regulating developmental and pathological angiogenesis[1][2]. ALK-1 Protein, Cynomolgus (HEK293, His) is produced in HEK293 cells with a C-Terminal His-tag. It consists of 118 amino acids (D22-Q118).
Background
ALK-1, also known as ACVRL1, is a type I receptor for TGF-β superfamily with 2 ligands, BMP9 and BMP10. ALK-1 is predominantly expressed in endothelial cells and plays a critical role in regulating angiogenesis[1][2].
Mature human ALK-1 shares 89% amino acid sequence identity with mouse and rat ALK-1. While, mouse ALK-1 shares 96% aa sequence identity with rat ALK-1 protein.
ALK-1 is able to bind to TGF-β1 or activins in the presence of either TβR-II or activin type II receptors, respectively. However, ALK-1 does not elicit a specific transcriptional response. Thus, ALK-1 has been considered an “orphan” receptor. ALK-1 is a type I receptor that mediates signaling of BMP9 (bone morphogenetic protein) and BMP10, proteins in the TGF-β superfamily. Signaling through ALK-1 results in phosphorylation of the intracellular Smad 1/5/8 cascade which activates proangiogenic transcription factors such as ID1 and ID3. ALK-1 binds to TGF-β1 and phosphorylates Smad1 and Smad5. Overexpression of ALK-1 in HepG2 cells inhibits the ALK5-mediated TGF-β1 response. The balance between ALK-1 and ALK5 may be crucial for controlling the properties of endothelium during angiogenesis[1]. BMP9/BMP10/ALK-1 signaling controlled the specific gene expression program and survival of Kupffer cells (KCs) through a Smad4-dependent pathway. Functionally, the loss of ALK-1 resulted in impaired capture of L. monocytogenes and overwhelming disseminated infections[2].
ALK-1 is expressed in blood vessels during embryogenesis and adult stages. In addition, mutations of the ALK-1 gene have been linked to the type II hereditary hemorrhagic telangiectasia[1]. ALK-1 inhibits BMP9-mediated Id-1 expression in human umbilical vein endothelial cells. In a chick chorioallantoic membrane assay, ALK-1 reduces VEGF-, FGF-, and BMP10-mediated vessel formation. In addition, ALK1 reduces tumor burden in mice receiving orthotopic grafts of MCF7 mammary adenocarcinoma cells[3].
In Vitro
Recombinant human ALK-1 (5 μg/mL; preincubated for 3 minutes) abolishes Hey1, Hey2 and Id2 genes induction by serum in primary human endothelial cells[4].
Verified Bioactivity
1.This product does not contain protein kinase domain.
2.Measured by its ability to inhibit BMP-9-induced alkaline phosphatase production by ATDC5 mouse chondrogenic cells. The ED50 for this effect is 3-12 ng/mL in the presence of 2 ng/mL of BMP-9.
MCE Validation Data
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Purity - SDS-PAGE
Purity - SDS-PAGE
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Bioactivity - Cell-Based Assay
Bioactivity - Cell-Based Assay
Technical Parameters
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Species Cynomolgus
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Source HEK293
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Tag C-His
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Accession
XP_005570958 (D22-Q118)
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Molecular Construction
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N-term
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ALK-1 (D22-Q118)
Accession # XP_005570958 -
His
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C-term
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Protein Length
Partial
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Synonyms
ACVRL1; TGF-B Superfamily Receptor Type I; Prev. ACVRLK1; ALK-1; Prev. ORW2; TSR-I; ALK1; SKR3; Serine/Threonine-Protein Kinase Receptor R3; Activin A Receptor Type II-Like Kinase 1 Variant 4; Activin Receptor-Like Kinase 1; Activin A Receptor Type II-Lik
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AA Sequence
DPVKPSRGPLVTCTCESPHCRGPTCQGAWCTVVLVREEGRHPQEHRGCGNLHRELCRGRPTEFVNHYCCDSHLCNRNVSLVLEATQTPSEQPGTDSQ
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Molecular Weight
Approximately 21-25 kDa due to the glycosylation.
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Purity
≥ 95%, as determined by reducing SDS-PAGE.
Product Properties
Lyophilized powder.
Lyophilized from a 0.22 μm filtered solution of PBS, pH 7.4.
<1 EU/μg, determined by LAL method.
It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH2O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).
Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.
Room temperature in continental US; may vary elsewhere.
Documentation
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Data Sheet (264 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
[1]. S P Oh, et al. Activin receptor-like kinase 1 modulates transforming growth factor-beta 1 signaling in the regulation of angiogenesis. Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2626-31. [Content Brief]
[2]. Dianyuan Zhao, et al. ALK1 signaling is required for the homeostasis of Kupffer cells and prevention of bacterial infection. J Clin Invest. 2022 Feb 1;132(3):e150489. [Content Brief]
[3]. Dianne Mitchell, et al. ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth. Mol Cancer Ther. 2010 Feb;9(2):379-88. [Content Brief]
[4]. Kerstin Wöltje, et al. Serum induces transcription of Hey1 and Hey2 genes by Alk1 but not Notch signaling in endothelial cells. PLoS One. 2015 Mar 23;10(3):e0120547. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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