Differential role of the JNK and p38 MAPK pathway in c-myc- and s-myc-mediated apoptosis

Kohji Noguchi, Hironobu Yamana, Chifumi Kitanaka, Toshihiro Mochizuki, Akiko Kokubu, Yoshiyuki Kuchino

研究成果: Article査読

43 被引用数 (Scopus)


The s-Myc is similar to c-Myc in its ability to induce apoptosis requiring caspase activation. However, s-Myc is distinct from c-Myc in that it has activity to suppress tumor growth and does not require wild-type p53 to induce apoptosis. These facts suggest differential regulation between s-Myc and c-Myc. Here we showed that s-Myc-mediated apoptosis triggered by UV was not inhibited by the inactive form mutant JNK (APF), though c-Myc-mediated apoptosis was. Moreover, we found that JNK did not affect the transactivation activity of s-Myc, but stimulated that of c-Myc. In contrast, both Myc-mediated apoptosis and caspase-3-like protease activation were suppressed by kinase-negative MKK6 and an inactive form mutant p38(AGF). Our results indicate that s-Myc does not require the JNK signaling unlike c-Myc during UV-triggered apoptosis, but the MKK6/p38MAPK pathway might regulate common apoptotic machinery for both s-Myc and c-Myc upstream of caspase. (C) 2000 Academic Press.

ジャーナルBiochemical and Biophysical Research Communications
出版ステータスPublished - 2000 1月 7

ASJC Scopus subject areas

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学


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