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ATM binds to -adaptin in cytoplasmic vesicles

机译:ATM与细胞质囊泡中的-adaptin结合

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摘要

Inherited mutations in the ATM gene lead to a complex clinical phenotype characterized by neuronal de- eneration, oculocutaneous telangiectasias, immune dysfunc- tion, and cancer predisposition. Using the yeast two-hybrid system, we demonstrate that ataxia telangiectasia mutated (ATM) binds to β-adaptin, one of the components of the AP-2 adaptor complex, which is involved in clathrin-mediated endocytosis of receptors. The interaction between ATM and β-adaptin was confirmed in vitro, and coimmunoprecipitation and colocalization studies show that the proteins also asso- ciate in vivo. ATM also interacts in vitro with β-NAP, a neuronal-specific β-adaptin homolog that was identified as an autoantigen in a patient with cerebellar degeneration.
机译:ATM基因的遗传突变会导致复杂的临床表型,其特征是神经元变性,眼皮肤毛细血管扩张,免疫功能低下和癌症易感性。使用酵母双杂交系统,我们证明了共济失调毛细血管扩张突变(ATM)绑定到AP-2适配器复杂,参与网格蛋白介导的受体内吞的组件之一的β-adaptin。在体外证实了ATM和β-适应素之间的相互作用,并且共免疫沉淀和共定位研究表明,蛋白质也与体内相关。 ATM还可以与β-NAP进行体外相互作用,β-NAP是一种神经元特异性β-adaptin同源物,在小脑变性患者中被鉴定为自身抗原。

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