RGD Reference Report - Activity deprivation-dependent induction of the proapoptotic BH3-only protein Bim is independent of JNK/c-Jun activation during apoptosis in cerebellar granule neurons. - Rat Genome Database

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

Authors: Shi, L  Gong, S  Yuan, Z  Ma, C  Liu, Y  Wang, C  Li, W  Pi, R  Huang, S  Chen, R  Han, Y  Mao, Z  Li, M 
Citation: Shi L, etal., Neurosci Lett. 2005 Feb 25;375(1):7-12. Epub 2004 Nov 24.
RGD ID: 2290487
Pubmed: PMID:15664113   (View Abstract at PubMed)
DOI: DOI:10.1016/j.neulet.2004.10.082   (Journal Full-text)

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.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of neuron apoptotic process  IMP 2290487 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Jun  (Jun proto-oncogene, AP-1 transcription factor subunit)


Additional Information