Cbl negatively regulates JNK activation and cell death
Cell Research, ISSN: 1001-0602, Vol: 19, Issue: 8, Page: 950-961
2009
- 12Citations
- 21Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations12
- Citation Indexes12
- 12
- CrossRef8
- Captures21
- Readers21
- 21
Article Description
Here, we explore the role of Cbl proteins in regulation of neuronal apoptosis. In two paradigms of neuron apoptosis nerve growth factor (NGF) deprivation and DNA damage cellular levels of c-Cbl and Cbl-b fell well before the onset of cell death. NGF deprivation also induced rapid loss of tyrosine phosphorylation (and most likely, activation) of c-Cbl. Targeting c-Cbl and Cbl-b with siRNAs to mimic their loss/inactivation sensitized neuronal cells to death promoted by NGF deprivation or DNA damage. One potential mechanism by which Cbl proteins might affect neuronal death is by regulation of apoptotic c-Jun N-terminal kinase (JNK) signaling. We demonstrate that Cbl proteins interact with the JNK pathway components mixed lineage kinase (MLK) 3 and POSH and that knockdown of Cbl proteins is sufficient to increase JNK pathway activity. Furthermore, expression of c-Cbl blocks the ability of MLKs to signal to downstream components of the kinase cascade leading to JNK activation and protects neuronal cells from death induced by MLKs, but not from downstream JNK activators. On the basis of these findings, we propose that Cbls suppress cell death in healthy neurons at least in part by inhibiting the ability of MLKs to activate JNK signaling. Apoptotic stimuli lead to loss of Cbl protein/activity, thereby removing a critical brake on JNK activation and on cell death. © 2009 IBCB, SIBS, CAS.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=68749112487&origin=inward; http://dx.doi.org/10.1038/cr.2009.74; http://www.ncbi.nlm.nih.gov/pubmed/19546888; https://www.nature.com/articles/cr200974; http://sciencechina.cn/gw.jsp?action=cited_outline.jsp&type=1&id=3654167&internal_id=3654167&from=elsevier; https://dx.doi.org/10.1038/cr.2009.74
Springer Science and Business Media LLC
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