Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation

Nature

Volumn 387, Issue 6632, 1997, Pages 516-519

  Baskaran, R ^a   Wood, L D ^a   Whitaker, L L ^a   Canman, C E ^b   Morgan, S E ^b   Xu, Y ^c   Barlow, C ^d   Baltimore, D ^c   Wynshaw Boris, A ^d   Kastan, M B ^b   Wang, J Y J ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b JOHNS HOPKINS UNIVERSITY   (United States)

^c MASSACHUSETTS INSTITUTE OF TECHNOLOGY   (United States)

^d NATIONAL INSTITUTES OF HEALTH   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN TYROSINE KINASE;

ARTICLE; ATAXIA TELANGIECTASIA; ENZYME ACTIVATION; GENE MUTATION; IONIZING RADIATION; PHOSPHORYLATION; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION;

3T3 CELLS; ANIMALS; ATAXIA TELANGIECTASIA; CELL CYCLE; CELL CYCLE PROTEINS; CELL LINE, TRANSFORMED; DNA-BINDING PROTEINS; ENZYME ACTIVATION; GAMMA RAYS; HUMANS; MICE; PROTEIN-SERINE-THREONINE KINASES; PROTEINS; PROTO-ONCOGENE PROTEINS C-ABL; RNA POLYMERASE II; TRANSFECTION; TUMOR SUPPRESSOR PROTEINS;

EID: 0030925565     PISSN: 00280836     EISSN: None     Source Type: Journal    
DOI: 10.1038/387516a0     Document Type: Article

References (25)

1. Savitsky, K. et al. The complete sequence of the coding region of the ATM gene reveals similarity to cell cycle regulators in different species. Hum. Mol. Genet. 4, 2025-2032 (1995).
2. Savitsky, K. et al. A single ataxia telangiectasia gene with a product similar to PI-3 kinase. Science 268, 1749-1753 (1995).
3. Barlow, C. et al. Atm-deficient mice: a paradigm of ataxia telangiectasia. Cell 86, 159-171 (1996).
4. Xu, Y. et al. Targeted disruption of ATM leads to growth retardation, chromosomal fragmentation during meiosis, immune defects and thymic lymphoma. Genes Dev. 10, 2411-2422 (1996).
5. Xu, Y. & Baltimore, D. Dual roles of ATM in the cellular response to radiation and in cell growth control. Genes Dev. 10, 2401-2410 (1996).
6. Kastan, M. B. et al. A mammalian cell cycle checkpoint utilizing p53 and GADD45 is defective in ataxia-telangiectasia. Cell 71, 587-597 (1992).
7. Liu, Z. G. et al. Three distinct signalling responses by marine fibroblasts to genotoxic stress. Nature 384, 273-276 (1996).
8. Kharbanda, S. et al. Activation of the c-Abl tyrosine kinase in the stress response to DNA-damaging agents. Nature 376, 785-788 (1995).
9. Canman, C. E., Wolff, A. C., Chen, C. Y., Fornace, A. J. & Kastan, M. B. The p53-dependent G1 cell cycle checkpoint pathway and ataxia-telangiectasia. Cancer Res. 54, 5054-5058 (1994).
10. Lu, X. & Lane, D. P. Differential induction of transcriptionally active p53 following UV or ionizing radiation: defects in chromosome instability syndromes? Cell 75, 765-778 (1993).
11. Khanna, K. K. & Lavin, M. F. Ionizing radiation and UV induction of p53 protein by different pathways in ataxia-telangiectasia cells. Oncogene 8, 3307-3312 (1993).
12. Baskaran, R., Chiang, G. G. & Wang, J. Y. J. Identification of a binding site in c-Abl tyrosine kinase for the C-terminal repeated domain of RNA polymerase II. Mol. Cell. Biol. 16, 3361-3369 (1996).
13. Siede, W., Allen, J. B., Elledge, S. J. & Friedberg, E. C. The Saccharomyces cerevisiae MEC1 gene, which encodes a homolog of the human ATM gene product, is required for G1 arrest following radiation treatment. J. Bacteriol. 178, 5841-5843 (1996).
14. Byrd, P. J. et al. Mutations revealed by sequencing the 5′ half of the gene for ataxia-telangiectasia. Hum. Mol. Genet. 5, 145-149 (1996).
15. Gilad, S. et al. Ataxia-telangiectasia: predominance of mutations that inactivate the ATM protein by truncations or large deletions. Hum. Mol. Genet. 5, 433-439 (1996).
16. Morgan, S. E., Lovly, C., Pandita, T. K., Shiloh, Y. & Kastan, M. B. Fragments of ATM which have dominant-negative or complementing activity. Mol. Cell. Biol. 17, 2020-2029 (1997).
17. Bannister, A. J., Gottlieb, T. M., Kouzarides, T. & Jackson, S. P. c-Jun is phosphorylated by the DNA-dependent protein kinase in vitro-definition of the minimal kinase recognition motif. Nucleic Acids Res. 21, 1289-1295 (1993).
18. Baskaran, R., Dahmus, M. E. & Wang, J. Y. J. Tyrosine phosphorylation of mammalian RNA polymerase II carboxyl-terminal domain. Proc. Natl Acad. Sci. USA 90, 11167-11171 (1993).
19. Yuan, Z.-M. et al. Role of c-Abl tyrosine kinase in growth arrest response to DNA damage. Nature 382, 272-274 (1996).
20. Painter, R. B. & Young, B. R. Radiosensitivity in ataxia-telangiectasia: a new explanation. Proc. Natl Acad. Sci. USA 77, 7315-7317 (1980).
21. Fornace, A. J. et al. Mammalian genes coordinately regulated by growth arrest signals and DNA-damaging agents. Mol. Cell. Biol. 9, 4196-4203 (1989).
22. Friedberg, E. C., Walker, G. C. & Siede, W. DNA Repair and Mutagenesis (ASM, Washington DC, 1995).
23. Sanchez, Y. et al. Regulation of RAD53 by the ATM-like kinases Mec1 and Tel1 in yeast cell cycle checkpoint pathways. Science 271, 357-360 (1996).
24. Welch, P. J. & Wang, J. Y. J. A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl tyrosine kinase in the cell cycle. Cell 75, 779-790 (1993).
25. Leonardo, A. D., Linke, S. P., Clarkin, K. & Wahl, G. M. DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts. Genes Dev. 8, 2540-2551 (1994).