Cosmo Bio抗体,Anti Latent TGF-Beta (Plasmin Degradation Fragment L57) pAb (Rabbit, Affinity Purified),CAC-RIK-CP-PT57

TGF-β作为一种原蛋白产生,其中25 kD活性TGF-β被一种称为潜伏期相关蛋白(LAP)的n端前肽捕获。在接受某些刺激后,潜在复合物中的构象变化被诱导,从而从复合物中释放活性TGF-β。

Anti Latent TGF-Beta (Plasmin Degradation Fragment L57) pAb (Rabbit, Affinity Purified),CAC-RIK-CP-PT57

Application: ELISA, WB

Clonality: Polyclonal

Host: Rabbit

Purification: Purified – Affinity

Reactivity: Human

TGF-β is produced as a pro-protein in which the 25 kD active TGF-β is trapped by an N-terminal pro-peptide called Latency Associated Protein (LAP). Upon receipt of certain stimuli a conformational change is induced in a latent complex to release the active TGF-β from the complex. The resultant TGF-β binds to cognate signaling receptors and exerts various physiological and pathological activities. This reaction is called TGF-β activation reaction, which is known to be induced by binding of the latent complex to cell adhesion proteins such as thrombospondin and integrins, and/or by being cleaved by the action of proteases such as serine proteases, cysteine proteases, and MMPs in an organ and context-depending manner. The RIKEN Center for Biomedical Science and Research Center for Liver Cancer Prevention and Research Unit focused on the involvement of the serine protease plasmin and plasma kallikrein in the release and activation of TGF-β and its involvement in liver diseases. They showed that plasmin and plasma kallikrein cleave, respectively, at 56Lys-57Leu and 58Arg-59Leu within the LAP portion of the latent TGF-β1 molecule. The anti-TGF-β1 LAP-degradates (LAP-D) antibodies are useful to investigate the molecular mechanism of TGF-β activation and its related diseases including liver fibrosis/cirrhosis and liver degeneration.

TGF-β作为一种原蛋白产生,其中25 kD活性TGF-β被一种称为潜伏期相关蛋白(LAP)的n端前肽捕获。在接受某些刺激后,潜在复合物中的构象变化被诱导,从而从复合物中释放活性TGF-β。由此产生的TGF-β与同源信号受体结合并发挥各种生理和病理活性。该反应被称为TGF-β激活反应,已知是由潜在复合物与细胞粘附蛋白(如血栓反应蛋白和整合素)结合诱导的,和/或由蛋白酶(如丝氨酸蛋白酶、半胱氨酸蛋白酶和基质金属蛋白酶)以器官和环境依赖的方式作用而裂解。RIKEN生物医学科学研究中心和肝癌预防研究中心重点研究丝氨酸蛋白酶纤溶酶和血浆激肽酶参与TGF-β的释放和激活及其在肝脏疾病中的作用。他们发现,在潜在TGF-β1分子的LAP部分内,纤溶酶和血浆激肽蛋白分别在56Lys-57Leu和58Arg-59Leu处裂解。抗TGF-β1 lap – degradation (LAP-D)抗体可用于研究TGF-β激活的分子机制及其相关疾病,包括肝纤维化/肝硬化和肝变性。