| 货号 | AF3956-SP |
| 别名 | BMP-10; bone morphogenetic protein 10; MGC126783 | 全称 | Bone Morphogenetic Protein 10 |
| 反应种属 | Human |
| 应用 | Western Blot(0.1 µg/mL) |
| 目标/特异性 | Detects human BMP‑10 propeptide in direct ELISAs and Western blots. In direct ELISAs, less than 1% cross-reactivity with mature recombinant human BMP-10 is observed. |
| 使用方法 | Western Blot: 0.1 µg/mL |
| 来源 | Reconstitute at 0.2 mg/mL in sterile PBS. |
| 产品组分 |
| 供应商 | R&D Systems |
| Entrez Gene IDs | 27302 (Human) |
| 纯化方式 | Antigen Affinity-purified |
| 免疫原 | Mouse myeloma cell line NS0-derived recombinant human BMP‑10 propeptide (R&D Systems, Catalog # 3956-BP) Ser20-Arg313 Accession # O95393 |
| 生物活性 | Human |
| 标记 | Unconjugated |
| 溶解方法 | Reconstitute at 0.2 mg/mL in sterile PBS. |
| 背景 | BMP-10, along with BMP-9, GDF-5, -6, and -7, belongs to a subgroup of sequence related TGF-beta superfamily proteins that signal through heterodimeric complexes composed of type I and type II BMP receptors (1 - 3). Proteolytic removal of the propeptide from the 60 kDa proprotein yields a 12 kDa mature BMP-10 which forms disulfide-linked non-glycosylated homodimers (4, 5). In transfectants, BMP-10 is secreted as a cleaved mature dimer, an uncleaved proform dimer, and an uncleaved proform monomer (4). The propeptide of human BMP-10 shares 82% amino acid sequence identity with mouse and rat proBMP-10 and 19% - 34% with the propeptides of human BMP-9, GDF-5, -6, and -7. BMP-10 is critical for the proper development of the heart and first appears at the onset of trabeculation and chamber formation (6 - 8). Homozygous BMP-10 knockout mice die in utero due to arrested cardiac development (7). BMP-10 is required for maintaining expression of the cardiogenic transcription factors NKX2.5 and MEF2C in developing myocardium and promoting the growth of embryonic cardiomyocytes (7, 9, 10). The BMP-10 mediated proliferation of these cells requires Notch signaling (11). NKX2.5 itself negatively regulates BMP-10 expression in cardiac myocytes (10). Multiple human congenital heart defects result from mutations in NKX2.5 and require BMP-10 expression (10). In mice, genetic knockout of ErbB leads to a similar phenotype but appears not to involve BMP-10, and knockout of the calcium channel subunit FKBP12 induces BMP-10 overexpression (7). BMP-10 in the postnatal heart promotes increased cardiomyocyte and heart size (8). BMP-10 has been shown to induce signaling through ALK-1, BMPR-IA, BMPR-IB, and BMPR-II in transfectants and non-cardiac cell lines (4, 5). A functional BMP-10 receptor in the heart has not yet been identified, although deletion of BMPR-IA or BMP-10 causes similar cardiac morphogenetic abnormalities (12). |
| 运输条件 | Blue Ice |
| 存放说明 | 4℃ |
| 参考文献 |
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