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- W3140030969 abstract "蛋白质酷氨酸磷酸酶 alpha (PTP ) 由 dephosphorylating Tyr527/530 作为 Src 的使活跃之物工作，一个批评否定规章的地点。PTP 催化活动的增加从 PTP/Grb2 建筑群在 Ser180 或 Ser204 和它的分离要求它的 phosphorylation。这里，我们证明表皮的生长因素(EGF ) 刺激增加 PTP 的能力在 BT-20 和 SKBR3 乳癌房间行由 dephosphorylating Tyr530 激活 Src。有 EGF 的这些房间的治疗短暂地减少了有 Grb2 的 PTP 和提高的 PTP 的协会经由被蛋白质 kinase C 三角洲(PKC ) 堵住的 Ser180 和 Ser204 phosphorylation 的催化活动禁止者 rottlerin 或由 siRNA 或由 PTPS180A/S204A 的 overexpression 的 PKC 击倒变异。PTP siRNA 在癌症房间堵住了调停 EGF 的 Src 激活并且在殖民地形成上禁止了，而控制 siRNA 不。这些结果建议 PTP 连接与 Src 激活发信号的表皮的生长因素受体(EGFR ) 的激活并且可以为乳癌的治疗提供一个新奇治疗学的目标。" @default.
- W3140030969 created "2021-04-13" @default.
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- W3140030969 date "2013-01-01" @default.
- W3140030969 modified "2023-09-23" @default.
- W3140030969 title "PTPα-mediated Src activation by EGF in human breast cancer cells" @default.
- W3140030969 hasPublicationYear "2013" @default.
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