2. 重组蛋白
  3. Cytokines and Growth Factors Receptor Proteins Enzymes & Regulators
  4. TGF-beta Superfamily Receptor Serine/Threonine Kinases Serine/Threonine Kinase Proteins
  5. Activin/Inhibins Receptor
  6. Activin A Receptor Type 2A (ACTR-IIA)

Activin A Receptor Type 2A (ACTR-IIA)  (激活素受体 ⅡA)

重组蛋白定制服务

ACVR2A，也称为激活素 RIIA，是一种激活素 II 型受体。在配体结合时，ACVR2A 可以形成由两种 II 型和两种 I 型跨膜丝氨酸/苏氨酸激酶组成的受体复合物。ACVR2A 是 Activin A、Activin B 和 Inhibin A 的受体。
来自不同物种的 ACVR2A 蛋白的氨基酸序列非常稳定，由此得出的结论是，在进化过程中，ACVR2A 只发生了轻微的变化，在人和动物体内，其功能是相似的。
激活素和 BMP 的信号传导是高度混杂的，因为除了通过 ALK4/7 信号传导外，激活素 II 型受体 (ACVR2A 和 2B) 还可以与几种 I 型 BMP 受体 (ALK1/2/3/6) 相互作用，这也可以与 II 型 BMP 受体 BMPRII 形成复合物。II 型受体磷酸化并激活自磷酸化的 I 型受体，然后结合并激活 SMAD 转录调节因子。ACVR2A 可以与不同的 I 型受体形成复合物，这些受体向 Smad2/3 (ALK4) 或 Smad1/5/8 (ALK2、ALK3、ALK6) 发出信号。不同的 I 型受体竞争与 ACVR2A 结合，这种竞争提供了一种机制，平衡激活素 A 介导的、ALK4 依赖性 Smad2/3 信号传导和 BMP 介导的 ALK2 或 ALK3 依赖性信号传导至 Smad1/5/8 之间的信号传导.在骨髓瘤细胞中，激活素 A 治疗可抑制 BMP-6 和 BMP-9 通过 ACVR2A/ACVR2B/ALK2 诱导的 SMAD1/5/8 活化[1][3]。

ACVR2A, also known as Activin RIIA, is an activin type II receptor. On ligand binding, ACVR2A can forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. ACVR2A is a receptor for Activin A, Activin B and Inhibin A.
The sequence of amino acids in ACVR2A proteins from different species is very stable, which leads to the conclusion that in the process of evolution, ACVR2A has been only slightly altered, and that both in humans and in animals, its function is similar.
Signaling by activins and BMPs is highly promiscuous, since apart from signaling through ALK4/7, the activin type II receptors (ACVR2A and 2B) can interact also with several type I BMP receptors (ALK1/2/3/6), which can also form complexes with the type II BMP receptor, BMPRII. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. ACVR2A can form complexes with different type I receptors that signal either to Smad2/3 (ALK4) or to Smad1/5/8 (ALK2, ALK3, ALK6). The different type I receptors compete for binding to ACVR2A and that this competition provides a mechanism that balances signaling between Activin A-mediated, ALK4-dependent Smad2/3 signaling, and BMP-mediated ALK2 or ALK3-dependent signaling to Smad1/5/8. In myeloma cells, BMP-6- and BMP-9-induced activation of SMAD1/5/8 through ACVR2A/ACVR2B/ALK2 is inhibited by activin A treatment[1][3].

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