Role of JNK activation in apoptosis: A double-edged sword

Jing Liu, Anning Lin*

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

384 Scopus citations


JNK is a key regulator of many cellular events, including programmed cell death (apoptosis). In the absence of NF-κB activation, prolonged JNK activation contributes to TNF-α induced apoptosis. JNK is also essential for UV induced apoptosis. However, recent studies reveal that JNK can suppress apoptosis in IL-3-dependent hematopoietic cells via phosphorylation of the proapoptotic Bcl-2 family protein BAD. Thus, JNK has pro- or antiapoptotic functions, depending on cell type, nature of the death stimulus, duration of its activation and the activity of other signaling pathways.

Original languageEnglish (US)
Pages (from-to)36-42
Number of pages7
JournalCell Research
Issue number1
StatePublished - 2005


  • Apoptosis
  • IL-3
  • JNK
  • NF-κB
  • TNF-α

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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