Dose rate and mode of exposure are key factors in JNK activation by UV irradiation

被引:33
作者
Adler, V
Polotskaya, A
Kim, J
Dolan, L
Davis, R
Pincus, M
Ronai, Z
机构
[1] AMER HLTH FDN,MOL CARCINOGENESIS PROGRAM,VALHALLA,NY 10595
[2] UNIV MASSACHUSETTS,HOWARD HUGHES MED INST,WORCESTER,MA 01605
[3] VET ADM MED CTR,DEPT PATHOL,BROOKLYN,NY 11209
关键词
D O I
10.1093/carcin/17.9.2073
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Single exposure of cells to UVC (254 nm for 30 s) or to UVB (300 nm for 10 min) was shown to activate jun-NH2 kinases which, in turn, phosphorylate their substrates ELK-1, c-jun and ATF-2, While UVC (40-80 J/m(2)) activates JNK up to 4 h, with maximal induction after 30 min, UVB (150-300 J/m(2)) activates JNK over a prolonged period, up to 24 h, with maximal induction after 6 h, UV-mediated activation of src-related tyrosine kinases and MAPK revealed different kinetics, with maximal induction after 24 h, As recent studies had indicated a role of a UVC component in mediating the ability of UVB to activate JNK, we have examined the effect of dose rate as well as of multiplicity of exposures on the activation of these kinases, The UVC portion found in 300 J/m(2) UVB (5%, corresponding to 15 J/m(2), administered within 10 s) did not activate JNK, However, when the same dose was administered at a lower rate (i.e. over 10 min, as needed for UVB irradiation) it was found capable of activating JNK, MAPK and src kinases, but to a lower degree and with different kinetics than found for UVB, Such differences point to cellular changes which are elicited by UVB, but not UVC, Although a single UVB exposure using a filter that blocks wavelengths below 300 nm prevented activation of JNK, multiple exposures of filtered UVB wavelengths (mimicking chronic exposure) were able to activate JNK, We conclude that the mode of UVB exposure (dose rate and multiplicity) is a crucial determinant for physiologically relevant activation of JNK.
引用
收藏
页码:2073 / 2076
页数:4
相关论文
共 29 条
  • [11] THE UV RESPONSE INVOLVING THE RAS SIGNALING PATHWAY AND AP-1 TRANSCRIPTION FACTORS IS CONSERVED BETWEEN YEAST AND MAMMALS
    ENGELBERG, D
    KLEIN, C
    MARTINETTO, H
    STRUHL, K
    KARIN, M
    [J]. CELL, 1994, 77 (03) : 381 - 390
  • [12] FORNACE AJ, 1992, ANNU REV GENET, V26, P505
  • [13] FUCHS S, 1996, IN PRESS ONCOGENE
  • [14] AN OSMOSENSING SIGNAL-TRANSDUCTION PATHWAY IN MAMMALIAN-CELLS
    GALCHEVAGARGOVA, Z
    DERIJARD, B
    WU, IH
    DAVIS, RJ
    [J]. SCIENCE, 1994, 265 (5173) : 806 - 808
  • [15] TRANSCRIPTION FACTOR ATF2 REGULATION BY THE JNK SIGNAL-TRANSDUCTION PATHWAY
    GUPTA, S
    CAMPBELL, D
    DERIJARD, B
    DAVIS, RJ
    [J]. SCIENCE, 1995, 267 (5196) : 389 - 393
  • [16] KASTAN MB, 1991, CANCER RES, V51, P6304
  • [17] WILD-TYPE P53 IS A CELL-CYCLE CHECKPOINT DETERMINANT FOLLOWING IRRADIATION
    KUERBITZ, SJ
    PLUNKETT, BS
    WALSH, WV
    KASTAN, MB
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (16) : 7491 - 7495
  • [18] THE STRESS-ACTIVATED PROTEIN-KINASE SUBFAMILY OF C-JUN KINASES
    KYRIAKIS, JM
    BANERJEE, P
    NIKOLAKAKI, E
    DAI, TA
    RUBIE, EA
    AHMAD, MF
    AVRUCH, J
    WOODGETT, JR
    [J]. NATURE, 1994, 369 (6476) : 156 - 160
  • [19] DIFFERENTIAL-EFFECTS BY THE P21 CDK INHIBITOR ON PCNA-DEPENDENT DNA-REPLICATION AND REPAIR
    LI, R
    WAGA, S
    HANNON, GJ
    BEACH, D
    STILLMAN, B
    [J]. NATURE, 1994, 371 (6497) : 534 - 537
  • [20] UV-RESPONSIVE ELEMENT (TGACAACA) FROM RAT FIBROBLASTS TO HUMAN MELANOMAS
    RONAI, Z
    RUTBERG, S
    YANG, YM
    [J]. ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, 1994, 23 (03) : 157 - 163