根据已发表的人类TβRI(Type I TGFβreceptor)基因序列设计2对引物,利用PCR扩增得到了1个长度为1512bp的TβRI基因全长序列。序列分析结果表明与数据库公布的人类序列(Genebank登录号:NM_004612)一致。通过基因工程的方法,构建含有ECF...根据已发表的人类TβRI(Type I TGFβreceptor)基因序列设计2对引物,利用PCR扩增得到了1个长度为1512bp的TβRI基因全长序列。序列分析结果表明与数据库公布的人类序列(Genebank登录号:NM_004612)一致。通过基因工程的方法,构建含有ECFP-TβRI-YFP融合蛋白的真核表达TβRI生物传感器载体。该载体转染293T细胞后能够稳定高效表达。结果表明构建的TβRI生物传感器载体能用于TGFβ信号通路中的功能研究。展开更多
Transforming growth factor-β （TGF-β） members are key cytokines that control embryogenesis and tissue homeostasis via transmembrane TGF-β type II （TβR II） and type I （TβRI） and serine/threonine kinases recep...Transforming growth factor-β （TGF-β） members are key cytokines that control embryogenesis and tissue homeostasis via transmembrane TGF-β type II （TβR II） and type I （TβRI） and serine/threonine kinases receptors. Aberrant activation of TGF-β signaling leads to diseases, including cancer. In advanced cancer, the TGF-β/SMAD pathway can act as an oncogenic factor driving tumor cell invasion and metastasis, and thus is considered to be a therapeutic target. The activity of TGF-β/SMAD pathway is known to be regulated by ubiquitination at multiple levels. As ubiquitination is reversible, emerging studies have uncovered key roles for ubiquitin-removals on TGF-β signaling components by deubiquitinating enzymes （DUBs）. In this paper, we summarize the latest findings on the DUBs that control the activity of the TGF-β signaling pathway. The regula- tory roles of these DUBs as a driving force for cancer progression as well as their underlying working mech- anisms are also discussed.展开更多
文摘根据已发表的人类TβRI(Type I TGFβreceptor)基因序列设计2对引物,利用PCR扩增得到了1个长度为1512bp的TβRI基因全长序列。序列分析结果表明与数据库公布的人类序列(Genebank登录号:NM_004612)一致。通过基因工程的方法,构建含有ECFP-TβRI-YFP融合蛋白的真核表达TβRI生物传感器载体。该载体转染293T细胞后能够稳定高效表达。结果表明构建的TβRI生物传感器载体能用于TGFβ信号通路中的功能研究。
文摘Transforming growth factor-β （TGF-β） members are key cytokines that control embryogenesis and tissue homeostasis via transmembrane TGF-β type II （TβR II） and type I （TβRI） and serine/threonine kinases receptors. Aberrant activation of TGF-β signaling leads to diseases, including cancer. In advanced cancer, the TGF-β/SMAD pathway can act as an oncogenic factor driving tumor cell invasion and metastasis, and thus is considered to be a therapeutic target. The activity of TGF-β/SMAD pathway is known to be regulated by ubiquitination at multiple levels. As ubiquitination is reversible, emerging studies have uncovered key roles for ubiquitin-removals on TGF-β signaling components by deubiquitinating enzymes （DUBs）. In this paper, we summarize the latest findings on the DUBs that control the activity of the TGF-β signaling pathway. The regula- tory roles of these DUBs as a driving force for cancer progression as well as their underlying working mech- anisms are also discussed.
