Recombinant Human TGFBR1/ALK-5 protein (His tag)
Price:
- 表达系统: E.coli
- 蛋白编码: P36897
别称 |
AAT5;ACVRLK4;ALK-5;ALK5;ESS1;LDS1;LDS1A;LDS2A;MSSE;SKR4;tbetaR-I;TGFR-1
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表达系统 |
E.coli
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序列 |
Leu 34-Leu 126
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蛋白编码 |
P36897
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种属 |
Human
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计算分子量 |
10.1 kDa
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表观分子量 |
30 kDa
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标签 |
N-His
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纯度 |
> 95 % as determined by reducing SDS-PAGE.
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内毒素 |
Please contact us for more information.
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保存条件 |
Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
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运输条件 |
This product is provided as lyophilized powder which is shipped with ice packs.
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制剂 |
Lyophilized from sterile PBS, pH 7.4.
Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization. Please refer to the specific buffer information in the printed manual. |
复溶方法 |
Please refer to the printed manual for detailed information.
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背景 |
Transforming growth factor, beta receptor I, also known as Transforming growth factor-beta receptor type I , Serine / threonine-protein kinase receptor R4, Activin receptor-like kinase 5, SKR4, ALK-5, and TGFBR1, is a single-pass type I membrane protein which belongs to the protein kinase superfamily and TGFB receptor subfamily. TGFBR1 / ALK-5 is found in all tissues examined. It is most abundant in placenta and least abundant in brain and heart. TGF-beta functions as a tumor suppressor by inhibiting the cell cycle in the G1 phase. Administration of TGF-beta is able to protect against mammary tumor development in transgenic mouse models in vivo. Disruption of the TGF-beta/SMAD pathway has been implicated in a variety of human cancers, with the majority of colon and gastric cancers being caused by an inactivating mutation of TGF-beta RII. On ligand binding, TGFBR1 / ALK-5 forms a receptor complex consisting of two type I I and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which auto-phosphorylate, then bind and activate SMAD transcriptional regulators. TGF-beta signaling via TGFBR1 / ALK-5 is not required in myocardial cells during mammalian cardiac development, but plays an irreplaceable cell-autonomous role regulating cellular communication, differentiation and proliferation in endocardial and epicardial cells. Defects in TGFBR1 / ALK-5 are the cause of Loeys-Dietz syndrome type 1A (LDS1A), Loeys-Dietz syndrome type 2A (LDS2A), and aortic aneurysm familial thoracic type 5 (AAT5).
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实验操作视频
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