Ultraviolet radiation, but not γ radiation or etoposide-induced DNA damage, results in the phosphorylation of the murine p53 protein at serine-389

被引:151
作者
Lu, H
Taya, Y
Ikeda, M
Levine, AJ
机构
[1] Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA
[2] Natl Canc Ctr, Res Inst, Div Biol, Chuo Ku, Tokyo 104, Japan
[3] MBL Co Ltd, Ina Labs, Nagano 396, Japan
关键词
D O I
10.1073/pnas.95.11.6399
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Polyclonal antibodies were produced and purified that selectively react with a p53 epitope containing the murine phosphoserine-389 or the human phosphoserine-392 residue, but not the unphosphorylated epitope, These antibodies, termed alpha 392, were employed to demonstrate that the phosphorylation of this serine-389 residue in the p53 protein occurs in vivo in response to ultraviolet radiation of cells containing the p53 protein. After ultraviolet radiation of cells in culture, p53 levels increase and concomitantly serine-389 is phosphorylated in these cells. By contrast, the serine-389 phosphorylation of the p53 protein was not detected by these antibodies in the increased levels of p53 protein made in response to gamma radiation or the treatment of cells with etoposide. These results demonstrate an ultraviolet responsive and specific phosphorylation site at serine-389 of the mouse or serine-392 of the human p53 protein. Previous studies have demonstrated that this phosphorylation of p53 activates the protein for specific DNA binding. This study demonstrates in vivo a unique phosphorylation site in the p53 protein that responds to a specific type of DNA damage.
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页码:6399 / 6402
页数:4
相关论文
共 19 条
  • [1] ABOUSSEKHRA A, 1995, CELL, V80, P858
  • [2] [Anonymous], 1988, Antibodies: A Laboratory Manual
  • [3] Atm-deficient mice: A paradigm of ataxia telangiectasia
    Barlow, C
    Hirotsune, S
    Paylor, R
    Liyanage, M
    Eckhaus, M
    Collins, F
    Shiloh, Y
    Crawley, JN
    Ried, T
    Tagle, D
    WynshawBoris, A
    [J]. CELL, 1996, 86 (01) : 159 - 171
  • [4] DUAL ROLE OF TFIIH IN DNA EXCISION-REPAIR AND IN TRANSCRIPTION BY RNA-POLYMERASE-II
    DRAPKIN, R
    REARDON, JT
    ANSARI, A
    HUANG, JC
    ZAWEL, L
    AHN, KJ
    SANCAR, A
    REINBERG, D
    [J]. NATURE, 1994, 368 (6473) : 769 - 772
  • [5] DUAL ROLES OF A MULTIPROTEIN COMPLEX FROM SACCHAROMYCES-CEREVISIAE IN TRANSCRIPTION AND DNA-REPAIR
    FEAVER, WJ
    SVEJSTRUP, JQ
    BARDWELL, L
    BARDWELL, AJ
    BURATOWSKI, S
    GULYAS, KD
    DONAHUE, TF
    FRIEDBERG, EC
    KORNBERG, RD
    [J]. CELL, 1993, 75 (07) : 1379 - 1387
  • [6] MONOCLONAL-ANTIBODIES SPECIFIC FOR SIMIAN VIRUS-40 TUMOR-ANTIGENS
    HARLOW, E
    CRAWFORD, LV
    PIM, DC
    WILLIAMSON, NM
    [J]. JOURNAL OF VIROLOGY, 1981, 39 (03) : 861 - 869
  • [7] HAU M, 1997, J BIOL CHEM, V271, P29380
  • [8] REGULATION OF THE CRYPTIC SEQUENCE-SPECIFIC DNA-BINDING FUNCTION OF P53 BY PROTEIN-KINASES
    HUPP, TR
    LANE, DP
    [J]. COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY, 1994, 59 : 195 - 206
  • [9] A MAMMALIAN-CELL CYCLE CHECKPOINT PATHWAY UTILIZING P53 AND GADD45 IS DEFECTIVE IN ATAXIA-TELANGIECTASIA
    KASTAN, MB
    ZHAN, QM
    ELDEIRY, WS
    CARRIER, F
    JACKS, T
    WALSH, WV
    PLUNKETT, BS
    VOGELSTEIN, B
    FORNACE, AJ
    [J]. CELL, 1992, 71 (04) : 587 - 597
  • [10] The consensus motif for phosphorylation by cyclin D1-Cdk4 is different from that for phosphorylation by cyclin A/E-Cdk2
    Kitagawa, M
    Higashi, H
    Jung, HK
    SuzukiTakahashi, I
    Ikeda, M
    Tamai, K
    Kato, J
    Segawa, K
    Yoshida, E
    Nishimura, S
    Taya, Y
    [J]. EMBO JOURNAL, 1996, 15 (24) : 7060 - 7069