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Cited by 194

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Mcl-1 Is a Key Regulator of Apoptosis during CNS Development and after DNA Damage

Open access
Arbour, N., Vanderluit, J. L., Le Grand, J. N., Jahani-Asl, A., Ruzhynsky, V. A., Cheung, E. C. C., Kelly, M. A., MacKenzie, A. E., Park, D. S., Opferman, J. T., Slack, R. S.·2008·Journal of Neuroscience

Abstract

Despite the importance of Mcl-1, an anti-apoptotic Bcl-2 family member, in the regulation of apoptosis, little is known regarding its role in nervous system development and injury-induced neuronal cell death. Because germline deletion of Mcl-1 results in peri-implantation lethality, we address the function of Mcl-1 in the nervous system using two different conditional Mcl-1 mouse mutants in the developing nervous system. Here, we show for the first time that Mcl-1 is required for neuronal development. Neural precursors within the ventricular zone and newly committed neurons in the cortical plate express high levels of Mcl-1 throughout cortical neurogenesis. Loss of Mcl-1 in neuronal progenitors results in widespread apoptosis. Double labeling with active caspase 3 and Tuj1 reveals that newly committed Mcl1 deficient neurons undergo apoptosis as they commence migration away from the ventricular zone. Examination of neural progenitor differentiation in vitro demonstrated that cell death in the absence of Mcl1 is cell autonomous. Although conditional deletion of Mcl-1 in cultured neurons does not trigger apoptosis, loss of Mcl-1 sensitizes neurons to an acute DNA damaging insult. Indeed, the rapid reduction of Mcl-1 mRNA and protein levels are early events after DNA damage in neurons, and maintaining high Mcl-1 levels can protect neurons against death. Together, our results are the first to demonstrate the requirement of Mcl-1, an anti-apoptotic Bcl-2 family protein, for cortical neurogenesis and the survival of neurons after DNA damage.

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Crossref · 10.1523/jneurosci.4940-07.2008

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Metadata

Authors
Arbour, N., Vanderluit, J. L., Le Grand, J. N., Jahani-Asl, A., Ruzhynsky, V. A., Cheung, E. C. C., Kelly, M. A., MacKenzie, A. E., Park, D. S., Opferman, J. T., & Slack, R. S.
Venue
Journal of Neuroscience
Published
2008-06-11
Volume
28
Issue
24
Pages
6068-6078
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W1992089991
Cited by
194
References
8
FWCI
3.23
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Mcl-1 Is a Key Regulator of Apoptosis during CNS Development and after DNA Damage. https://app.cochat.ai/papers/10.1523/jneurosci.4940-07.2008
The paper
Arbour, N., Vanderluit, J. L., Le Grand, J. N., Jahani-Asl, A., Ruzhynsky, V. A., Cheung, E. C. C., Kelly, M. A., MacKenzie, A. E., Park, D. S., Opferman, J. T., & Slack, R. S. (2008). Mcl-1 Is a Key Regulator of Apoptosis during CNS Development and after DNA Damage. Journal of Neuroscience. https://doi.org/10.1523/jneurosci.4940-07.2008

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.