Function and sequence analyses of tumor suppressor gene p53 of CHO.K1 cells

DNA and Cell Biology

Volumn 18, Issue 4, 1999, Pages 315-321

  Tzang, Bor Show ^a   Lai, Yi Chyi ^a   Hsu, Mandy ^a   Chang, Hsueh Wei ^a   Chang, Chia Chin ^a   Huang, Pien C ^a   Liu, Yin Chang ^a  

^a NATIONAL TSING HUA UNIVERSITY   (Taiwan)

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN P53;

ANIMAL CELL; ARTICLE; CELL CYCLE; CHO CELL; DNA REPAIR; GENOME; HUMAN; HUMAN CELL; NONHUMAN; PRIORITY JOURNAL; TUMOR SUPPRESSOR GENE; ULTRAVIOLET IRRADIATION;

3T3 CELLS; ANIMALS; CHO CELLS; CRICETINAE; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLINS; G1 PHASE; GENE EXPRESSION; GENES, TUMOR SUPPRESSOR; HUMANS; INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS; MICE; POINT MUTATION; PROTEIN BIOSYNTHESIS; PROTEINS; SEQUENCE ANALYSIS, DNA; TRANSFECTION; TUMOR SUPPRESSOR PROTEIN P53; X-RAYS;

ANIMALIA; CRICETINAE; CRICETULUS GRISEUS;

EID: 0032947349     PISSN: 10445498     EISSN: None     Source Type: Journal    
DOI: 10.1089/104454999315376     Document Type: Article

References (28)

1. ALADJEM, M.I., SPIKE, B.T., RODEWALD, L.W., HOPE, T.J., KLEMM, M., JAENISCH, R., and WAHL, G.M. (1998). ES cells do not activate p53-dependent stress responses and undergo p53-independent apoptosis in response to DNA damage. Curr. Biol. 8, 145-155.
2. BURATOWSKI, S., and CHODOSH, L.A. (1996). DNA-protein interactions. In Current Protocols in Molecular Biology. F.M. Ausubel, R. Brent, R.E. Kingston, D.D. Moore, J.G. Seidman, J.A. Smith, and K. Struhl, eds. (John Wiley and Sons. Inc. New York, NY) pp. 12.2.5-6.
3. BARAK, Y., JUVEN, T., HAFFNER, R., and OREN, M. (1993). mdm2 expression is induced by wild type p53 activity. EMBO J. 12, 461-468.
4. CANMAN, C.E., GILMER, T.M., COUTTS, S.B., and KASTAN, M.B. (1995). Growth factor modulation of p53-mediated growth arrest versus apoptosis. Genes Dev. 9, 600-611.
5. CHO, Y., GORINA, S., JEFFREY, P.D., and PAVLETICH, N.P. (1994). Crystal structure of a p53 tumor suppressor-DNA complex: understanding tumorigenic mutations. Science 265, 346-355.
6. EL-DEIRY, W.S., KERN, S.E., PIETENPOL, J.A., KINZLER, K.W., and VOLGELSTEIN, B. (1992). Definition of a consensus binding site for p53. Nature Genet. 1, 45-49.
7. EL-DEIRY, W.S., HARPER, J.W., O'CONNOR, P.M., VELCULESCU, V.E., CANMAN, C.E., JACKMAN, J., PIETENPOL, J.A., BURRELL, M., HILL, D.E., WANG, Y., WIMAN, K.G., MERCER, W.E., KASTAN, M.B., KOHN, K.W., ELLEDGE, SJ., KINZLER, K.W., and VOGELSTEIN, B. (1994). WAF1/CIP1 is induced in p53-mediated G1 arrest and apoptosis. Cancer Res. 54, 1169-1174.
8. FINLAY, C.A., HINDS, P.W., and LEVINE, A.J. (1989). The p53 proto-oncogene can act as a suppressor of transformation. Cell 57, 1083-1093.
9. GORMAN, C.M., MOFFAT, L.M., and HOWARD, B.M. (1982). Recombinant genomes which express chloramphenicol acetyltransferase in mammalian cells. Mol. Cell. Biol. 2, 1044-1051.
10. HAWKINS, D.S., DEMERS, G.W., and GALLOWAY, D.A. (1996). Inactivation of p53 enhances sensitivity to multiple chemotherapeutic agents. Cancer Res. 56, 892-898.
11. HSU, Y.-S., TANG, F.-M., LIU, W.-L., CHUANG, J.-Y., LAI, M.-Y., and LIN, Y.-S. (1995). Transcriptional regulation by p53: functional interactions among multiple regulatory domains. J. Biol. Chem. 270, 6966-6974.
12. HUANG, D.Y., and PRYSTOWSKY, M.B. (1996). Identification of an essential cis-element near the transcription start site for transcriptional activation of the proliferating cell nuclear antigen gene. J. Biol. Chem. 271, 1218-1225.
13. KAO, F.-T., FAIK, P., and PUCK, T.T. (1979). Extension of branching processes from hybrids of brain and Chinese hamster ovary cells. Exp. Cell Res. 122, 83-91.
14. KASTAN, M.B., ZHANG, D.-W., CARRIER, F., JACKS, T., WASH, W.V., PLUNKETT, B.S., VOGELSTEIN, B., and FORNACE, A.J. (1992). A mammalian cell cycle checkpoint pathway utilizing p53 and gadd 45 is defective in ataxia-telangiectasia. Cell 71, 587-597.
15. KERN, S.E., KINZLER, K.W., BRUSKIN, A., JAROSZ, D., FRIEDMAN, P., PRIVES, C., and VOLGELSTEIN, B. (1991). Identification of p53 as a sequence-specific DNA binding protein. Science 252, 1708-1711.
16. LARNER, J.M., LEE, H., and HAMLIN, J.L. (1994). Radiation effects on DNA synthesis in a defined chromosomal replicon. Mol. Cell. Biol. 14, 1901-1908.
17. LEE, H., LARNER, J.M., and HAMLIN, J.L. (1997). Cloning and characterization of Chinese hamster p53 cDNA. Gene 184, 177-183.
18. LEVINE, A.J. (1997). p53, the cellular gatekeeper for growth and division. Cell 88, 323-331.
19. MICHALOVITZ, D., HALEVY, O., and OREN, M. (1990). Conditional inhibition of transformation and of cell proliferation by a temperature-sensitive mutant of p53. Cell 62, 671-680.
20. MOMAND, J., ZAMBETTI, G.P., OLSON, D.C., GEORGE, D., and LEVINE, A.J. (1992). The mdm2 oncogene product forms a complex with the p53 protein and inhibits p53 mediated transactivation. Cell 69, 1237-1245.
21. NAGAICH, A.K., APPELLA, E., and HARRINGTON, R.E. (1997). DNA bending is essential for the site-specific recognition of DNA response elements by the DNA binding domain of the tumor suppressor protein p53. J. Biol. Chem. 272, 14842-14849.
22. ORY, K., LEGROS, Y., AUGUIN, C., and SOUSSI, T. (1994). Analysis of the most representative tumour-derived p53 mutants reveals that changes in protein conformation are not correlated with loss of transactivation or inhibition of cell proliferation. EMBO J. 13, 3496-3504.
23. SAMBROOK, J., FRITSCH, E.F., and MANIATIS, T. (1989). In Molecular Cloning: A Laboratory Manual. (Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY) pp. 18.51-18.75.
24. TSUTSUMI-ISHII, Y., TADOKORO, K., HANAOKA, F., and TSUCHIDA, N. (1995). Response of heat shock element within the human hsp70 promoter to mutated p53 genes. Cell Growth Differ. 6, 1-8.
25. SCHEFFNER, M., WERNESS, B.A., HUIBREGTSE, J.M., LEVINE, A.J., and HOWLEY, P.M. (1990). The E6 oncoprotein encoded by human papillomaviruses type 16 and 18 promotes the degradation of p53. Cell 63, 1129-1136.
26. ZAMBETTI, G.P., BARGONETTI, J., WALKER, K., PRIVES, C., and LEVINE, A.J. (1992). Wild-type p53 mediates positive regulation of gene expression through a specific DNA sequence element. Genes Dev. 6, 1143-1152.
27. ZAMBETTI, G.P., and LEVINE, A.J. (1993). A comparison of the biological activities of wild-type and mutant p53. FASEB J. 7, 855-865.
28. ZHAN, Q., CHEN, I.T., ANTINORE, M.J., and FORNACE. A.J., JR. (1998). 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.