Derailed endocytosis:emerging;feature;cance
2009-05-26 20:36:09 来源： 作者： 评论：0 点击：
Derailed endocytosis: an emerging feature of cancer
Abstract
Once engaged by soluble or matrix-anchored ligands, cell surface proteins are commonly sorted to lysosomal degradation through several endocytic pathways. Defective vesicular trafficking of growth factor receptors, as well as unbalanced recycling of integrin- and cadherin-based adhesion complexes, has emerged in the past 5 years as a multifaceted hallmark of malignant cells. In line with the cooperative nature of endocytic machineries, multiple oncogenic alterations underlie defective endocytosis, such as altered ubiquitylation (Cbl and Nedd4 ubiquitin ligases, for example), altered cytoskeletal interactions and alterations to Rab family members. Pharmaceutical interception of the propensity of tumour cells to derail their signalling and their adhesion receptors may constitute a novel target for cancer therapy.
异常的细胞内吞作用：癌症的一个新特征
摘要
一旦溶解配基或者基质固定配基参与，细胞表面蛋白一般通过几个细胞内吞途径被溶酶体降解。在过去的5年里，恶性细胞中生长因子受体的小泡运输的的缺陷，整联蛋白和钙粘蛋白的复合体循环利用的不平衡，已经作为多方面的标志被发现了。与细胞内吞作用机制的合作性质相一致，多重的致癌作用，是在有缺陷的内吞作用为基础条件下发挥作用的，比如变异的泛素（例如Cbl和Nedd4泛素链接酶），变异的细胞支架间的相互作用，Rab家族成员的变异。通过药物阻断肿瘤细胞这种倾向，改变其信号和黏着受体可能构成癌症治疗方面的一个新的目标。
Abstract
Once engaged by soluble or matrix-anchored ligands, cell surface proteins are commonly sorted to lysosomal degradation through several endocytic pathways. Defective vesicular trafficking of growth factor receptors, as well as unbalanced recycling of integrin- and cadherin-based adhesion complexes, has emerged in the past 5 years as a multifaceted hallmark of malignant cells. In line with the cooperative nature of endocytic machineries, multiple oncogenic alterations underlie defective endocytosis, such as altered ubiquitylation (Cbl and Nedd4 ubiquitin ligases, for example), altered cytoskeletal interactions and alterations to Rab family members. Pharmaceutical interception of the propensity of tumour cells to derail their signalling and their adhesion receptors may constitute a novel target for cancer therapy.
异常的细胞内吞作用：癌症的一个新特征
摘要
一旦溶解配基或者基质固定配基参与，细胞表面蛋白一般通过几个细胞内吞途径被溶酶体降解。在过去的5年里，恶性细胞中生长因子受体的小泡运输的的缺陷，整联蛋白和钙粘蛋白的复合体循环利用的不平衡，已经作为多方面的标志被发现了。与细胞内吞作用机制的合作性质相一致，多重的致癌作用，是在有缺陷的内吞作用为基础条件下发挥作用的，比如变异的泛素（例如Cbl和Nedd4泛素链接酶），变异的细胞支架间的相互作用，Rab家族成员的变异。通过药物阻断肿瘤细胞这种倾向，改变其信号和黏着受体可能构成癌症治疗方面的一个新的目标。
相关热词搜索：
上一篇：半数多发性硬化患者应用干扰素疗法可减少病灶
下一篇：特异性EGFR突变影响吉非替尼单药治疗效果
频道总排行
医学推广
频道本月排行
热门购物
评论排行
- 2011年临床执业医师考试实践技能真...(13)
- 腋臭手术视频(12)
- 2008年考研英语真题及参考答案(5)
- 节食挑食最伤女人的免疫系统(5)
- 核辐射的定义和单位(5)
- CKD患者Tm与IMT相关(5)
- 齐鲁医院普外科开展“喉返神经监护...(5)
- windows7激活工具WIN7 Activation v1.7(5)
- 正常微循环(5)
- 美大学性教育课来真的 男女上阵亲...(4)
