ATM binds to beta-adaptin in cytoplasmic vesicles.

Published

Journal Article

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 beta-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 beta-adaptin was confirmed in vitro, and coimmunoprecipitation and colocalization studies show that the proteins also associate in vivo. ATM also interacts in vitro with beta-NAP, a neuronal-specific beta-adaptin homolog that was identified as an autoantigen in a patient with cerebellar degeneration. Our data describing the association of ATM with beta-adaptin in vesicles indicate that ATM may play a role in intracellular vesicle and/or protein transport mechanisms.

Full Text

Duke Authors

Cited Authors

  • Lim, DS; Kirsch, DG; Canman, CE; Ahn, JH; Ziv, Y; Newman, LS; Darnell, RB; Shiloh, Y; Kastan, MB

Published Date

  • August 18, 1998

Published In

Volume / Issue

  • 95 / 17

Start / End Page

  • 10146 - 10151

PubMed ID

  • 9707615

Pubmed Central ID

  • 9707615

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.95.17.10146

Language

  • eng

Conference Location

  • United States