ACVR2B 蛋白, Mouse (HEK293, His-hFc)

ACVR2B is a type II member of the TGF-β family of receptor Serine/Threonine kinases. ACVR2B binds to activins and growth differentiation factors (GDF), which in turn activate type I receptors, activating downstream molecule SMAD2/3^[1]. ACVR2B Protein, Mouse (HEK293, His-hFc) is produced in HEK293 cells with a C-Terminal His-tag and a C-Terminal Fc-tag. It consists of 134 amino acids (M1-T134).

2B 型激活素受体 (ACVR2B)，也称为 ActR-IIB 和 MGC116908，是一种 II 型激活素受体。I 型受体对于信号传导至关重要；结合配体和表达 I 型受体需要 II 型受体^[1]。
不同物种的 ACVR2B 蛋白的氨基酸序列非常稳定，这导致结论是，在进化过程中，ACVR2B仅发生了轻微改变，无论是在人类还是动物中，其功能都是相似的。
激活素和生长分化因子（GDF）与ACVR2B结合，进而激活类型I 受体，如激活素受体样激酶 (ALK) ALK4 和 ALK5，激活下游分子 SMAD2/3。SMADS 调节许多肌原基因，例如 myoD、肌细胞生成素和 Myf5，这些基因参与细胞肥大、增殖或分化。非经典 ACVR2B 通路也被证明可以调节 MAP 激酶。ACVR2B 阻断肌生长抑制素、其密切同源物 GDF11 以及激活素 A、激活素 B 和 BMP10^[1] 的信号传导。激活素 A 主要与 1 型受体 ALK4 或 ALK7 结合，与 ACVR2A 或 ACVR2B 形成复合物，从而激活 SMAD2 或 SMAD3^[2]。
在骨髓瘤细胞中，BMP-6- 和 BMP激活素 A 处理可抑制 -9 通过 ACVR2A/ACVR2B/ALK2 诱导的 SMAD1/5/8 激活^[2]。ACVR2B 已被证明可以在肿瘤宿主中保留肌肉质量并延长生存时间，并在成骨不全和肌营养不良模型中增加骨量^[3]。

Recombinant mouse ACVR2B (2 ng/mL; added 3 min before hypoxia) antagonizes SMAD2 signaling and cell death in cardiomyocytes that are subjected to hypoxic stress^[1].

Recombinant mouse ACVR2B (1 mg/kg; s.c.; once) shows cardioprotection activity in ischemia-reperfusion (IR) injury mouse. ACVR2B= modifies cardiac metabolism, left ventricular mitochondrial respiration, as well as cardiac phenotype toward physiological hypertrophy. By blocking myostatin, ACVR2B potentially reduces cardiomyocyte death and modifies cardiomyocyte metabolism for hypoxic conditions to protect the heart from IR injury^[1].

Mouse

HEK293

C-hFc;C-His

P27040-1 (S19-T134)

11481  [NCBI]

60-65 kDa

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

<1 EU/μg, determined by LAL method.

• [1]. Johanna Magga, et al. Systemic Blockade of ACVR2B Ligands Protects Myocardium from Acute Ischemia-Reperfusion Injury. Mol Ther. 2019 Mar 6;27(3):600-610.  [Content Brief]

  [2]. Oddrun Elise Olsen, et al. Activin A inhibits BMP-signaling by binding ACVR2A and ACVR2B. Cell Commun Signal. 2015 Jun 6;13:27.  [Content Brief]

  [3]. Rafael Barreto, et al. ACVR2B/Fc counteracts chemotherapy-induced loss of muscle and bone mass. Sci Rep. 2017 Oct 31;7(1):14470.  [Content Brief]