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ATM binds to β-adaptin in cytoplasmic vesicles

By Dae-Sik Lim, David G. Kirsch, Christine E. Canman, Jin-Hyun Ahn, Yael Ziv, Lori S. Newman, Robert B. Darnell, Yosef Shiloh and Michael B. Kastan

Abstract

Inherited mutations in the ATM gene lead to a complex clinical phenotype characterized by neuronal degeneration, oculocutaneous telangiectasias, immune dysfunction, 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 associate 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. Our data describing the association of ATM with β-adaptin in vesicles indicate that ATM may play a role in intracellular vesicle and/or protein transport mechanisms

Topics: Biological Sciences
Publisher: The National Academy of Sciences
Year: 1998
OAI identifier: oai:pubmedcentral.nih.gov:21476
Provided by: PubMed Central
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