ATM binds to beta-adaptin in cytoplasmic vesicles

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.
Publisher
NATL ACAD SCIENCES
Issue Date
1998-08
Language
ENG
Keywords

ATAXIA-TELANGIECTASIA CELLS; CYCLE CHECKPOINT PATHWAY; ALPHA-ADAPTIN; PROTEIN; CLATHRIN; GENE; RECEPTOR; PRODUCT; DYNAMIN; P53

Citation

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.95, no.17, pp.10146 - 10151

ISSN
0027-8424
DOI
10.1073/pnas.95.17.10146
URI
http://hdl.handle.net/10203/74819
Appears in Collection
BS-Journal Papers(저널논문)
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