BMPR1A/ALK-3 蛋白, Human (HEK293, His)

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.

ALK-3（BMPR1A；ACVRLK3）是骨形态发生蛋白（BMP）I 型受体，针对 BMP2、BMP4、GDF5 和 GDF6。BMP I 型受体中，ALK-2 和 3 广泛表达于组织中，而 ALK-1 在内皮细胞 (EC) 中选择性表达^[1]。铁调素是铁代谢的主要调节剂，由肝细胞合成和释放，以响应体内铁浓度增加和炎症。BMP/ALK/SMAD 通路控制铁调素表达，而 BMP I 型受体 ALK-2 和 ALK-3 分别负责铁依赖性铁调素上调和基础铁调素表达，以避免低铁调素导致铁超载或高铁调素水平导致铁超载。诱导铁限制性红细胞生成^[2]。ALK-3 通过 GDF5 相互作用正向调节软骨细胞分化，并介导 GDF6^[3] 诱导脂肪生成。ALK-3 蛋白具有启动软骨形成、调节软骨形成谱系分化以及软骨内骨形成的功能^[5]。BMP 信号传导的组成部分与肺动脉高压 (PAH) 和内皮间质转化 (EndoMT) 的发病机制有关，并且 BMPR1A 是维持内皮特性和防止过度 EndoMT 的关键。BMPR1A-ID2/ZEB1-TGFBR2 信号轴可作为 PAH 和其他 EndoMT 相关血管疾病的潜在新靶点^[4]。

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].

Human

HEK293

C-His

P36894 (Q24-R152)

657  [NCBI]

28-33 kDa

Greater than 85% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [1]. Yang P, et al. The role of bone morphogenetic protein signaling in vascular calcification. Bone. 2020 Dec;141:115542.  [Content Brief]

  [2]. Traeger L, et al. HFE and ALK3 act in the same signaling pathway. Free Radic Biol Med. 2020 Nov 20;160:501-505.  [Content Brief]

  [3]. Miyazawa K, et al. Regulation of TGF-β Family Signaling by Inhibitory Smads. Cold Spring Harb Perspect Biol. 2017 Mar 1;9(3):a022095.  [Content Brief]

  [4]. Lee HW, et al. BMPR1A Promotes ID2-ZEB1 Interaction to Suppress Excessive Endothelial to Mesenchymal Transition. Cardiovasc Res. 2022 Sep 27:cvac159.  [Content Brief]

  [5]. Jing J, et al. Bmpr1a Signaling in Cartilage Development and Endochondral Bone Formation. Vitam Horm. 2015;99:273-91.  [Content Brief]

  [6]. Wu XG, et al. HFE interacts with the BMP type I receptor ALK3 to regulate hepcidin expression. Blood. 2014 Aug 21;124(8):1335-43.  [Content Brief]