Code | CSB-MP001260HU1 |
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A DNA fragment encoding the 20-135aa of human ACVR2A was fused with the 10xHis-tag at the C-terminus and expressed in mammalian cells through a vector. The resulting product is the recombinant human ACVR2A protein. It carries a C-terminal 10xHis-tag. Its purity exceeds 95% as determined by SDS-PAGE. It has been validated to be an active protein in a functional ELISA, where immobilized human ACVR2A at 2 μg/mL can bind the anti-ACVR2A recombinant antibody (CSB-RA623829MA1HU), with the EC50 of 3.848-4.375 ng/mL.
The ACVR2A protein is a multifunctional receptor that integrates signals from the TGF-β superfamily to regulate a wide array of biological functions, including muscle growth, immune responses, and skeletal development. It is integral to signaling pathways that regulate cellular proliferation, differentiation, and apoptosis, thereby influencing tissue homeostasis and development [1][2].
ACVR2A mainly regulates muscle growth and differentiation. It is activated by activins, myostatin, and BMPs, which are crucial for muscle development and maintenance [2]. Furthermore, ACVR2A signaling has been implicated in the pathophysiology of various diseases, including cancer and fibrosis. ACVR2A has been shown to mediate the effects of activin A in promoting fibrotic processes in liver diseases, particularly through its interaction with hepatic stellate cells [3]. This highlights its role in inflammation and tissue remodeling, which are critical in chronic disease states.
ACVR2A also modulates immune responses. It is involved in the differentiation of T-helper cells, particularly Th17 cells, which are known to contribute to autoimmune conditions [3]. The signaling pathways activated by ACVR2A can lead to both pro-inflammatory and anti-inflammatory responses, depending on the context and the ligands involved [4].
Moreover, ACVR2A is essential for proper skeletal development and homeostasis. It mediates signaling pathways that are crucial for bone formation and remodeling, and its dysregulation can lead to skeletal disorders [5]. Its involvement in both normal physiological processes and pathological conditions makes it a significant focus of research for therapeutic interventions in diseases such as cancer, fibrosis, and autoimmune disorders.
References:
[1] A. Kulminski, L. He, I. Culminskaya, Y. Loika, Y. Kernogitski, K. Arbeev, et al. Pleiotropic associations of allelic variants in a 2q22 region with risks of major human diseases and mortality, Plos Genetics, vol. 12, no. 11, p. e1006314, 2016. https://doi.org/10.1371/journal.pgen.1006314
[2] T. Bhattacharya, R. Shukla, R. Chatterjee, & S. Bhanja. Comparative analysis of silencing expression of myostatin (mstn) and its two receptors (acvr2a and acvr2b) genes affecting growth traits in knock down chicken, Scientific Reports, vol. 9, no. 1, 2019. https://doi.org/10.1038/s41598-019-44217-z
[3] H. Zhou, B. Ju, Y. Nie, B. Song, Y. Xu, & P. Gao. Adenovirus‑mediated knockdown of activin a receptor type�2a attenuates immune‑induced hepatic fibrosis in mice and inhibits interleukin‑17‑induced activation of primary hepatic stellate cells, International Journal of Molecular Medicine, 2018. https://doi.org/10.3892/ijmm.2018.3600
[4] C. Li, Z. Xu, X. Fan, H. Chen, Q. Yu, S. Fang, et al. Microrna-21 mediates the protective effects of mesenchymal stem cells derived from ipscs to human bronchial epithelial cell injury under hypoxia, Cell Transplantation, vol. 27, no. 3, p. 571-583, 2018. https://doi.org/10.1177/0963689718767159
[5] Y. Totoki, A. Yoshida, F. Hosoda, H. Nakamura, N. Hama, K. Ogura, et al. Unique mutation portraits and frequent col2a1 gene alteration in chondrosarcoma, Genome Research, vol. 24, no. 9, p. 1411-1420, 2014. https://doi.org/10.1101/gr.160598.113
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