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首页> 外文期刊>Cancer Cell >The Tensin-3 protein, including its SH2 domain, is phosphorylated by Src and contributes to tumorigenesis and metastasis.
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The Tensin-3 protein, including its SH2 domain, is phosphorylated by Src and contributes to tumorigenesis and metastasis.

机译:Tensin-3蛋白(包括其SH2结构域)被Src磷酸化,并有助于肿瘤发生和转移。

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摘要

In cell lines from advanced lung cancer, breast cancer, and melanoma, endogenous tensin-3 contributes to cell migration, anchorage-independent growth, and tumorigenesis. Although SH2 domains have not been reported previously to be phosphorylated, the tensin-3 SH2 domain is a physiologic substrate for Src. Tyrosines in the SH2 domain contribute to the biological activity of tensin-3, and phosphorylation of these tyrosines can regulate ligand binding. In a mouse breast cancer model, tensin-3 tyrosines are phosphorylated in a Src-associated manner in primary tumors, and experimental metastases induced by tumor-derived cell lines depend on endogenous tensin-3. Thus, tensin-3 is implicated as an oncoprotein regulated by Src and possessing an SH2 domain with a previously undescribed mechanism for the regulation of ligand binding.
机译:在晚期肺癌,乳腺癌和黑素瘤的细胞系中,内源性tensin-3有助于细胞迁移,非锚定生长和肿瘤发生。尽管以前没有报道SH2结构域被磷酸化,但tensin-3 SH2结构域是Src的生理底物。 SH2结构域中的酪氨酸有助于tensin-3的生物学活性,这些酪氨酸的磷酸化可调节配体结合。在小鼠乳腺癌模型中,原发性肿瘤中以Src相关的方式使tensin-3酪氨酸磷酸化,而肿瘤衍生的细胞系诱导的实验转移依赖于内源性tensin-3。因此,tensin-3被认为是一种受Src调控的癌蛋白,具有一个SH2结构域,具有之前未描述的调控配体结合的机制。

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