ATF-2 is preferentially activated by stress-activated protein kinases to mediate c-jun induction in response to genotoxic agents.

Documenti analoghi

• The level of intracellular glutathione is a key regulator for the induction of stress-activated signal transduction pathways including Jun N-terminal protein kinases and p38 kinase by alkylating agents.
  di: Wilhelm, D, et al.
  Pubblicazione: (1997)
• Heterodimer formation of cJun and ATF-2 is responsible for induction of c-jun by the 243 amino acid adenovirus E1A protein.
  di: van Dam, H, et al.
  Pubblicazione: (1993)
• Transcription of the protein kinase C-δ gene is activated by JNK through c-Jun and ATF2 in response to the anticancer agent doxorubicin
  di: Min, Byong Wook, et al.
  Pubblicazione: (2008)
• Anisomycin Selectively Desensitizes Signalling Components Involved in Stress Kinase Activation and fos and jun Induction
  di: Hazzalin, Catherine A., et al.
  Pubblicazione: (1998)
• Interleukin 1 induction of the c-jun promoter.
  di: Muegge, K, et al.
  Pubblicazione: (1993)