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.
Duke Scholars
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- Vero Cells
- Tumor Suppressor Proteins
- Transfection
- Saccharomyces cerevisiae
- Proteins
- Protein Serine-Threonine Kinases
- Protein Binding
- Phosphoproteins
- Peptide Fragments
- Nerve Tissue Proteins
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Vero Cells
- Tumor Suppressor Proteins
- Transfection
- Saccharomyces cerevisiae
- Proteins
- Protein Serine-Threonine Kinases
- Protein Binding
- Phosphoproteins
- Peptide Fragments
- Nerve Tissue Proteins