BMPRIB/ALK-6 蛋白, Mouse (HEK293, Fc)

BMPR1B/ALK-6 protein is a type I member of the bone morphogenetic protein (BMP) receptor family of transmembrane serine/threonine kinases^[1]. BMPR1B/ALK-6 is the receptor for BMP-7/OP-1 and GDF-5, positively regulates chondrocyte differentiation through GDF-5 interaction^[2][3]. BMPR1B/ALK-6 also involves in SCUBE3/BMP-2/BMP-4 signals regulation, controlling growth, morphogenesis, and bone and teeth development^[4]. ALK-6/GDF-9/BMP-15 signals is essential in prolificacy of goat^[5]. The mouse BMPR1B/ALK-6 protein contains 502 amino acids and a transmembrane domain (127-148 a.a.). BMPRIB/ALK-6 Protein, Mouse (HEK293, Fc) is produced by HEK293 cells (K14-K126) with C-terminal hFc-tag.

BMPRIB/ALK-6，也称为 CDw293（分化簇 w293），是跨膜丝氨酸/苏氨酸激酶的骨形态发生蛋白 (BMP) 受体家族的成员。BMP 参与软骨内骨形成和胚胎发生，通过形成两种类型 BMP 受体的异聚复合物来转导信号：I 型受体 (50-55 kD) 和 II 型受体 (70-80 kD)。II 型受体磷酸化并激活 I 型受体，I 型受体自身磷酸化，然后结合并激活 SMAD 转录调节因子^[1]。ALK-6 是 BMP-7/OP-1 和 GDF-5 的受体，通过 GDF-5 相互作用正向调节软骨细胞分化^[2][3]。ALK-6 信号传导还受 BMP-2/BMP-4 共受体 SCUBE3 控制，将 BMP 受体复合物招募到筏微域中，并可能通过增强 BMP 和 BMP I 型受体之间的特异性相互作用来正向调节信号传导^[3]。ALK-6 通过调节 BMP 信号传导参与控制生长、形态发生以及骨骼和牙齿发育，对于体内软骨形成至关重要，而 BMPR1A/ALK-3 和 ALK-6 在早期软骨形成过程中具有重叠功能^[4] 。ALK-6/GDF-9/BMP-15 信号在繁殖中发挥关键作用。ALK-6 和 GDF-9 广泛表达于 20 种组织中，其中卵巢表达最高，而 BMP-15 基因仅在卵巢和垂体中表达^[5]。ALK-6的序列在不同物种之间高度保守，小鼠的序列分别与人类（98.2%）和大鼠（99.0%）具有较高的相似性。

BMPR1B^-/-mice, exhibits cumulus expansion impairment and endometrial development defect, indicating female reproductive senescence^[7].

Measured by its ability to inhibit rhBMP-4-induced alkaline phosphatase production by ATDC5 mouse chondrogenic cells. The ED₅₀ for this effect is 0.1346 µg/mL in the presence of 30 ng/mL of rhBMP-4. Corresponding to a specific activity is 7.429×10³ U/mg.

• 
  Measured by its ability to inhibit rhBMP-4-induced alkaline phosphatase production by ATDC5 mouse chondrogenic cells. The ED₅₀ for this effect is 0.1346 µg/mL in the presence of 30 ng/mL of rhBMP-4.corresponding to a specific activity is 7.429×10³ U/mg.

Mouse

HEK293

C-hFc

P36898 (K14-K126)

12167  [NCBI]

KKEDGESTAPTPRPKILRCKCHHHCPEDSVNNICSTDGYCFTMIEEDDSGMPVVTSGCLGLEGSDFQCRDTPIPHQRRSIECCTERNECNKDLHPTLPPLKDRDFVDGPIHHK

Approximately 39.4 kDa.

• 
  Greater than 95% as determined by reducing SDS-PAGE.

无菌粉末

Lyophilized from a 0.2 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. 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.

• [1]. ten Dijke P, et al. Signaling via hetero-oligomeric complexes of type I and type II serine/threonine kinase receptors. Curr Opin Cell Biol. 1996 Apr;8(2):139-45.  [Content Brief]

  [2]. Xu H, et al. [BMP7 signaling via BMPR1A, BMPR1B inhibits the proliferation of lung large carcinoma NCI-H460 cell]. Zhongguo Fei Ai Za Zhi. 2010 Jul;13(7):659-64. Chinese.  [Content Brief]

  [3]. Demirhan O, et al. A homozygous BMPR1B mutation causes a new subtype of acromesomelic chondrodysplasia with genital anomalies. J Med Genet. 2005 Apr;42(4):314-7.  [Content Brief]

  [4]. Lin YC, et al. SCUBE3 loss-of-function causes a recognizable recessive developmental disorder due to defective bone morphogenetic protein signaling. Am J Hum Genet. 2021 Jan 7;108(1):115-133.  [Content Brief]

  [5]. Yang CX, et al. Cloning and mRNA expression levels of GDF9, BMP15, and BMPR1B genes in prolific and non-prolific goat breeds. Mol Reprod Dev. 2012 Jan;79(1):2.  [Content Brief]

  [6]. Yoon BS, et al. Bmpr1a and Bmpr1b have overlapping functions and are essential for chondrogenesis in vivo. Proc Natl Acad Sci U S A. 2005 Apr 5;102(14):5062-7.  [Content Brief]

  [7]. Renault L, et al. BMPR1A and BMPR1B Missense Mutations Cause Primary Ovarian Insufficiency. J Clin Endocrinol Metab. 2020 Apr 1;105(4):dgz226.  [Content Brief]