protein

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

HY-P7484

10 μg;50 μg

55;150 USD

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

proteins

HEK293

10 μg;50 μg

55;150 USD

406167998

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, Fc-His) is produced in HEK293 cells and has 129 amino acids (Q24-R152), with C-terminal Fc and His-tags.

Human

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] .

Bone morphogenetic protein receptor type-1A; ALK-3; SKR5; CD292; ACVRLK3; BMPR-IA

Greater than 95% as determined by reducing SDS-PAGE

Lyophilized after extensive dialysis against PBS, pH 7.4.

Room temperature in continental US; may vary elsewhere.