REGULATION OF C-JUN AP-1 EXPRESSION IN RAT L6 MYOBLASTS

被引:2
|
作者
THINAKARAN, G [1 ]
BAG, J [1 ]
机构
[1] UNIV GUELPH, DEPT MOLEC BIOL & GENET, GUELPH N1G 2W1, ONTARIO, CANADA
关键词
MYOGENIN; PROTEIN KINASE-C; CAMP; CA2+; MUSCLE DIFFERENTIATION;
D O I
10.1139/o93-031
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Myogenic differentiation of skeletal myoblasts in culture is triggered by withdrawal of serum mitogens. Expression of one of the serum-inducible, immediate early genes, the protooncogene c-jun, is maintained under low-serum conditions during myogenic differentiation of L6 myoblasts. In this report we have used agents that modulate protein kinases and Ca2+ levels to investigate how the expression of c-jun and myogenin mRNA and also the activator protein 1 (AP-1) DNA-binding activity are regulated in differentiating L6 cells. Our results show that expression of c-jun and myogenin are regulated independent of each other. Furthermore, down regulation of c-jun expression does not cause an increase in myogenin expression, suggesting that c-jun does not suppress myogenin expression in these cells. Electrophoretic mobility shift and ultraviolet cross-linking analyses revealed that the AP-1 complexes of proliferating myoblasts and differentiating myotubes are formed of similar set of polypeptides, and the AP- 1 binding activity is probably modulated by posttranslational modifications in differentiating L6 cells.
引用
收藏
页码:197 / 204
页数:8
相关论文
共 50 条
  • [41] Lysophosphatidylcholine phosphorylates CREB and c-jun and activates jun2TRE and AP-1 sites of c-jun promoter in vascular endothelial cells
    Ueno, Y
    Kume, N
    Nishi, E
    Ochi, H
    Moriwaki, H
    Kita, T
    [J]. CIRCULATION, 1998, 98 (17) : 380 - 380
  • [42] FOLLICLE-STIMULATING-HORMONE REGULATION OF AP-1 - INHIBITION OF C-JUN AND STIMULATION OF JUN-B GENE-TRANSCRIPTION IN THE RAT SERTOLI-CELL
    HAMIL, KG
    CONTI, M
    SHIMASAKI, S
    HALL, SH
    [J]. MOLECULAR AND CELLULAR ENDOCRINOLOGY, 1994, 99 (02) : 269 - 277
  • [43] Transcriptional regulation of Zic3 by heterodimeric AP-1(c-Jun/c-Fos) during Xenopus development
    Sung-Young Lee
    Hyun-Shik Lee
    Jin-Soo Moon
    Jong-Il Kim
    Jae-Bong Park
    Jae-Yong Lee
    Mae Ja Park
    Jaebong Kim
    [J]. Experimental & Molecular Medicine, 2004, 36 : 468 - 475
  • [44] Transcriptional regulation of Zic3 by heterodimeric AP-1(c-Jun/c-Fos) during Xenopus development
    Lee, SY
    Lee, FS
    Moon, JS
    Kim, JI
    Park, JB
    Lee, JY
    Park, MJ
    Kim, J
    [J]. EXPERIMENTAL AND MOLECULAR MEDICINE, 2004, 36 (05): : 468 - 475
  • [45] Role of the AP-1 transcription factor c-Jun in developing, adult and injured brain
    Raivich, Gennadij
    Behrens, Axel
    [J]. PROGRESS IN NEUROBIOLOGY, 2006, 78 (06) : 347 - 363
  • [46] c-Jun (AP-1) activates BMP-4 transcription in Xenopus embryos
    Knöchel, S
    Schuler-Metz, A
    Knöchel, W
    [J]. MECHANISMS OF DEVELOPMENT, 2000, 98 (1-2) : 29 - 36
  • [47] GLUCOCORTICOID REGULATION OF C-FOS, C-JUN AND TRANSCRIPTION FACTOR AP-1 IN THE ATT-20 CORTICOTROPE CELL
    AUTELITANO, DJ
    [J]. JOURNAL OF NEUROENDOCRINOLOGY, 1994, 6 (06) : 627 - 637
  • [48] Activation of AP-1 by okadaic acid in mouse keratinocytes associated with hyperphosphorylation of c-jun
    Peng, JX
    Bowden, GT
    Domann, FE
    [J]. MOLECULAR CARCINOGENESIS, 1997, 18 (01) : 37 - 43
  • [49] The Function of Heterodimeric AP-1 Comprised of c-Jun and c-Fos in Activin Mediated Spemann Organizer Gene Expression
    Lee, Sung-Young
    Yoon, Jaeho
    Lee, Hyun-Shik
    Hwang, Yoo-Seok
    Cha, Sang-Wook
    Jeong, Chul-Ho
    Kim, Jong-Il
    Park, Jae-Bong
    Lee, Jae-Yong
    Kim, SungChan
    Park, Mae Ja
    Dong, Zigang
    Kim, Jaebong
    [J]. PLOS ONE, 2011, 6 (07):
  • [50] Preincubation with sodium ascorbate potentiates insulin-dependent PKB/Akt and c-Jun phosphorylation in L6 rat myoblasts challenged with reactive oxygen/nitrogen species
    Orzechowski, A
    Lokociejewska, M
    Pawlikowska, P
    Kruszewski, M
    [J]. LIFE SCIENCES, 2005, 77 (05) : 496 - 511