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

Research output: Contribution to journalArticlepeer-review

41 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)221-227
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume267
Issue number1
DOIs
Publication statusPublished - 2000 Jan 7

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'Differential role of the JNK and p38 MAPK pathway in c-myc- and s-myc-mediated apoptosis'. Together they form a unique fingerprint.

Cite this