ALK-1 Protein, Human (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, Human (HEK293, His) is produced in HEK293 cells with a C-Terminal His-tag. It consists of 118 amino acids (M1-Q118).
- Species: Human
- Source: HEK293
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Storage:Stored at -80°C for 1 year from date of receipt. It is stable at -20°C for 3 months after opening. It is recommended to freeze aliquots at -80°C for extended storage. Avoid repeated freeze-thaw cycles.
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, Human (HEK293, His) is produced in HEK293 cells with a C-Terminal His-tag. It consists of 118 amino acids (M1-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 BMP9 induced alkaline phosphatase production by MC3T3E1 mouse chondrogenic cells. The ED50 for this effect is typically 40 ng/mL in the presence of 2 ng/mL of recombinant human BMP9.
Technical Parameters
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Species Human
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Source HEK293
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Tag C-His
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Accession
P37023 (D22-Q118)
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Molecular Construction
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N-term
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ALK-1 (D22-Q118)
Accession # P37023 -
His
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C-term
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Protein Length
Extracellular Domain
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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
DPVKPSRGPLVTCTCESPHCKGPTCRGAWCTVVLVREEGRHPQEHRGCGNLHRELCRGRPTEFVNHYCCDSHLCNHNVSLVLEATQPPSEQPGTDGQ
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Predicted Molecular Mass
12.3 kDa
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Molecular Weight
Approximately 27 kDa, based on SDS-PAGE under reducing conditions, due to the glycosylation.
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Glycosylation
Yes
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Purity
≥ 90%, as determined by reducing SDS-PAGE.
Product Properties
Solution
Supplied as a 0.2 μm filtered solution of PBS, pH 7.4.
<1 EU/μg, determined by LAL method.
Please use rapid thawing with running water to thaw the protein.
Stored at -80°C for 1 year from date of receipt. It is stable at -20°C for 3 months after opening. It is recommended to freeze aliquots at -80°C for extended storage. Avoid repeated freeze-thaw cycles.
Shipping with dry ice.
Documentation
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Data Sheet (264 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 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)