Genomic instability in Gadd45a-deficient mice

Nature Genetics

Volumn 23, Issue 2, 1999, Pages 176-184

  Hollander, M Christine ^a   Sheikh, M Saeed ^a   Bulavin, Dmitry V ^a   Lundgren, Karen ^b   Augeri Henmueller, Laura ^a   Shehee, Ronald ^b   Molinaro, Thomas A ^a   Kim, Kate E ^a   Tolosa, Eva ^a   Ashwell, Jonathan D ^a   Rosenberg, Michael P ^b   Zhan, Qimin ^a   Fernández Salguero, Pedro M ^a   Morgan, William F ^c,d   Deng, Chu Xia ^e   Fornace Jr , Albert J ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b GLAXOSMITHKLINE   (United States)

^c UNIVERSITY OF CALIFORNIA   (United States)

^d LAWRENCE BERKELEY NATIONAL LABORATORY   (United States)

^e NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN P53;

ANEUPLOIDY; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CENTROSOME; CHROMOSOME ABERRATION; CONTROLLED STUDY; CYTOKINESIS; EXENCEPHALY; GENE AMPLIFICATION; GENE TARGETING; GROWTH REGULATION; MITOSIS INHIBITION; MOUSE; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; RADIATION CARCINOGENESIS;

NON-PROGRAMMATIC;

ANIMALS; APOPTOSIS; CELL AGING; CELL CYCLE; CELL DIVISION; CELL TRANSFORMATION, NEOPLASTIC; CENTROSOME; EMBRYO; FEMALE; FIBROBLASTS; G1 PHASE; GAMMA RAYS; GENE DELETION; GENES, RAS; INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; NEOPLASMS; PHENOTYPE; PROTEINS; THYMUS HYPERPLASIA;

ANIMALIA; RODENTIA;

EID: 0344604528     PISSN: 10614036     EISSN: None     Source Type: Journal    
DOI: 10.1038/13802     Document Type: Article

References (30)

1. Kastan, M.B. et al. A mammalian cell cycle checkpoint utilizing p53 and GADD45 is defective in ataxia telangiectasia. Cell 71, 587-597 (1992).
2. Zhan, Q., Chen, I.T., Antinore, M.J. & Fornace, A.J. Jr Tumor suppressor p53 can participate in transcriptional induction of the GADD45 promoter in the absence of direct DNA binding. mol. Cell. Biol. 18, 2768-2778 (1998).
3. Amundson, S.A., Myers, T.G. & Fornace, A.J. Jr Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress. Oncogen 17, 3287-3300 (1998).
4. Harkin, D.P. et al. Induction of GADD45 and JNK/SAPK-dependent apoptosis following inducible expression of BRCA1. Cell 97, 575-586 (1999).
5. Donehower, L.A. et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nature 356, 215-221 (1992).
6. Sah, V.P. et al. A subset of p53-deficient embryos exhibit exencephaly. Nature Genet. 10, 175-180 (1995).
7. Ko, L.J. & Prives, C. p53: puzzle and paradigm. Genes Dev. 10, 1054-1072 (1996).
8. CIP/WAF1 undergo normal development, but are defective in G1 checkpoint control. Cell 82, 675-684 (1995).
9. Brugarolas, J. et al. Radiation-induced cell cycle arrest compromised by p21 deficiency. Nature 377, 552-557 (1995).
10. Smith, M.L. et al. Interaction of the p53-regulated protein Gadd45 with proliferating cell nuclear antigen. Science 266, 1376-1380 (1994).
11. Cip1. Oncogene 11, 1675-1683 (1995).
12. Takekawa, M. & Saito, H. A family of stress-inducible GADD45-like proteins mediate activation of the stress-responsive MTK1/MEKK4 MAPKKK. Cell 95, 521-530 (1998).
13. Zhan, Q. et al. Association with Cdc2 and inhibition of Cdc2/cyclin B1 kinase activity by the p53-regulated protein Gadd45. Oncogene 18, 2892-2900 (1999).
14. Carrier, F. et al. Gadd45, a p53-responsive stress protein, modifies DNA accessibility on damaged chromatin. Mol. Cell. Biol. 19, 1673-1685 (1999).
15. 2-M cell cycle checkpoint. Proc. Natl Acad. Sci. USA 96, 3706-3711 (1999).
16. Livingstone, L.R. et al. Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53. Cell 70, 923-935 (1992).
17. ARF. Cell 91, 649-659 (1997).
18. Zimmerman, W., Sparks, C.A. & Doxsey, S.J. Amorphous no longer: the centrosome comes into focus. Curr. Opin. Cell Biol. 11, 122-128 (1999).
19. Pockwinse, S.M. et al. Cell cycle independent interaction of CDC2 with the centrosome, which is associated with the nuclear matrix-intermediate filament scaffold. Proc. Natl Acad. Sci. USA 94, 3022-3027 (1997).
20. Fero, M.L., Randel, E., Gurley, K.E., Roberts, J.M. & Kemp, C.J. The murine gene p27Kip1 is haplo-insufficient for tumour suppression. Nature 396, 177-180 (1998).
21. Kemp, C.J., Wheldon, T. & Balmain, A. p53-deficient mice are extremely susceptible to radiation-induced tumorigenesis. Nature Genet. 8, 66-69 (1994).
22. Bouffler, S.D., Kemp, C.J., Balmain, A. & Cox, R. Spontaneous and ionizing radiation-induced chromosomal abnormalities in p53-deficient mice. Cancer Res. 55, 3883-3889 (1995).
23. Bunz, F. et al. Requirement for p53 and p21 to sustain G2 arrest after DNA damage. Science 282, 1497-1501 (1998).
24. Knudson, C.M., Tung, K.S., Tourtellotte, W.G., Brown, G.A. & Korsmeyer, S.J. Baxdef icient mice with lymphoid hyperplasia and male germ cell death. Science 270, 96-99 (1995).
25. Serrano, M., Lin, A.W., McCurrach, M.E., Beach, D. & Lowe, S.W. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell 88, 593-602 (1997).
26. Hendzel, M.J. et al. Mitosis-specific phosphorylation of histone H3 initiates primarily within pericentromeric heterochromatin during G2 and spreads in an ordered fashion coincident with mitotic chromosome condensation. Chromosoma 106, 348-360 (1997).
27. Hennings, H. et al. Calcium regulation of growth and differentiation of mouse epidermal cells in culture. Cell 19, 245-254 (1980).
28. Lowe, S.W., Schmitt, E.M., Smith, S.W., Osborne, B.A. & Jacks, T. p53 is required for radiation-induced apoptosis in mouse thymocytes. Nature 362, 847-849 (1993).
29. Nelson-Rees, WA., Hunter, L., Darlington, G.J. & O'Brien, S.J. Characteristics of HeLa strains: permanent vs. variable features. Cytogenet. Cell Genet. 27, 216-231 (1980).
30. Wang, X. Gorospe, M. & Holbrook, NJ. gadd45 is not required for activation of c-jun N-terminal kinase or p38 during acute stress. J. Biol. Chem. (in press).