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  6. BMPR1A/ALK-3 Protein, Human (HEK293, His)

BMPR1A/ALK-3 Protein, Human (HEK293, His)

Cat. No.: HY-P75594
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BMPR1A/ALK-3 protein (ACVRLK3) is the receptor bone morphogenetic protein (BMP) type I receptors, widely expressed in tissues. BMPR1A/ALK-3 protein mediates iron metabolism factor hepcidin expression, interacts with GDF5/6 to regulate chondrocyte differentiation and adipogenesis. BMPR1A-ID2/ZEB1-TGFBR2 signaling axis could serve as a potentia target for pulmonary arterial hypertension (PAH) and other endothelial-mesenchymal transition (EndoMT)-related vascular disorders. Human BMPR1A/ALK-3 has a full length of 532 a.a., with a motif (107-109 a.a.) mediating specificity for BMP ligand. BMPR1A/ALK-3 Protein, Human (HEK293, His) is produced in HEK293 cells, with a C-terminal His-tags.

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Description

BMPR1A/ALK-3 protein (ACVRLK3) is the receptor bone morphogenetic protein (BMP) type I receptors, widely expressed in tissues[1]. BMPR1A/ALK-3 protein mediates iron metabolism factor hepcidin expression, interacts with GDF5/6 to regulate chondrocyte differentiation and adipogenesis[2][3]. BMPR1A-ID2/ZEB1-TGFBR2 signaling axis could serve as a potentia target for pulmonary arterial hypertension (PAH) and other endothelial-mesenchymal transition (EndoMT)-related vascular disorders[4]. Human BMPR1A/ALK-3 has a full length of 532 a.a., with a motif (107-109 a.a.) mediating specificity for BMP ligand. BMPR1A/ALK-3 Protein, Human (HEK293, His) is produced in HEK293 cells, with a C-terminal His-tags.

Background

ALK-3 (BMPR1A; ACVRLK3) is the receptor bone morphogenetic protein (BMP) type I receptors, for BMP2, BMP4, GDF5 and GDF6. Among BMP type I receptors, ALK-2 and 3 are widely expressedin tissues, while ALK-1 is more selectively expressed in endothelial cells (ECs)[1]. Hepcidin, the main regulator of iron metabolism, is synthesized and released by hepatocytes in response to increased body iron concentration and inflammation. BMP/ALK/SMAD pathway controls hepcidin expression, while BMP type I receptors ALK-2 and ALK-3 are responsible for iron-dependent hepcidin upregulation and basal hepcidin expression, respectively, to avoid low hepcidin which causes iron overload or high hepcidin levels which induce iron-restricted erythropoiesis[2]. ALK-3 positively regulates chondrocyte differentiation through GDF5 interaction and mediates induction of adipogenesis by GDF6[3]. ALK-3 protein shows function for the initiation of chondrogenesis, for regulating differentiation along the chondrogenic lineage, and for endochondral bone formation[5]. Components of BMP signaling have been implicated in both pathogenesis of pulmonary arterial hypertension (PAH) and endothelial-mesenchymal transition (EndoMT), and BMPR1A is key to maintain endothelial identity and to prevent excessive EndoMT. BMPR1A-ID2/ZEB1-TGFBR2 signaling axis could serve as a potential novel target for PAH and other EndoMT-related vascular disorders[4].

In Vitro

ALK3-Flag (2 ng/mL; 48 h) synergizes with HFE, results phospho-Smad1/5/8, HA increasing and stimulates hepcidin expression in transfected Hep3B cells[6].

Species

Human

Source

HEK293

Tag

C-His

Accession

P36894 (Q24-R152)

Gene ID

657  [NCBI]

Molecular Construction
N-term
BMPR1A (Q24-R152)
Accession # P36894
His
C-term
Synonyms
ALK-3; BMPR­IA; Bone morphogenetic protein receptor type-1A; SKR5; CD292
Molecular Weight

28-33 kDa

Purity

Greater than 85% as determined by reducing SDS-PAGE

Endotoxin Level

<1 EU/μg, determined by LAL method.

Documentation
References
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Specific Activity (Unit/mg) = 106 ÷ Biological Activity (ED50)

Specific Activity (Unit/mg) = 106 ÷ Biological Activity (ED50)
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BMPR1A/ALK-3 Protein, Human (HEK293, His)
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