Activity deprivation-dependent induction of the proapoptotic BH3-only protein Bim is independent of JNK/c-Jun activation during apoptosis in cerebellar granule neurons

Leyu Shi, Shoufang Gong, Zhongmin Yuan, Chi Ma, Yanling Liu, Chuanfu Wang, Wenming Li, Rongbiao Pi, Shoujian Huang, Ruzhu Chen, Yifan Han, Zixu Mao, Mingtao Li

Research output: Journal article publicationJournal articleAcademic researchpeer-review

21 Citations (Scopus)


Bcl-2-interacting mediator of cell death (Bim), a proapoptotic BH3-only protein, plays a critical role in neuronal apoptosis. Cerebellar granule neurons (CGNs) depend on activity for their survival and undergo apoptosis when deprived of depolarizing concentration of KCl. While it has been proposed that the activation of c-Jun NH2-terminal protein kinase (JNK)/c-Jun pathway contributes to the upregulation of bim gene in neurons subjected to survival signaling withdrawal, here we show that neither inhibition of JNK activity nor expression of dominant-negative c-Jun suppresses the expression of bim gene induced by activity deprivation in CGNs. We conclude that induction of bim gene is independent of the activation of JNK/c-Jun signaling pathway by activity deprivation during apoptosis of CGNs.
Original languageEnglish
Pages (from-to)7-12
Number of pages6
JournalNeuroscience Letters
Issue number1
Publication statusPublished - 25 Feb 2005
Externally publishedYes


  • Apoptosis
  • Bim
  • c-Jun NH2-terminal protein kinase
  • Cerebellar granule neurons

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this