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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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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.[1]

References

  1. ATM binds to beta-adaptin in cytoplasmic vesicles. Lim, D.S., Kirsch, D.G., Canman, C.E., Ahn, J.H., Ziv, Y., Newman, L.S., Darnell, R.B., Shiloh, Y., Kastan, M.B. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
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