Blm-s , a BH3-Only Protein Enriched in Postmitotic Immature Neurons, Is Transcriptionally Upregulated by p53 during DNA Damage
Cell Reports, ISSN: 2211-1247, Vol: 9, Issue: 1, Page: 166-179
2014
- 6Citations
- 18Captures
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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.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations6
- Citation Indexes6
- CrossRef4
- Captures18
- Readers18
- 18
Article Description
Programmed cell death is a pivotal process that regulates neuronal number during development. Key regulators of this process are members of the BCL-2 family. Using mRNA differential display, we identified a Bcl-2 family gene, Blm-s ( Bcl-2 -like molecule, short form), enriched in postmitotic neurons of the developing cerebral cortex. BLM-s functions as a BH3-only apoptosis sensitizer/derepressor and causes BAX-dependent mitochondria-mediated apoptosis by selectively binding to prosurvival BCL-2 or MCL-1. When challenged with γ-irradiation that produces DNA double-strand breaks (DSBs), Blm-s is transcriptionally upregulated in postmitotic immature neurons with concurrently increased apoptosis. RNAi-mediated depletion of Blm-s protects immature neurons from irradiation-induced apoptosis. Furthermore, Blm-s is a direct target gene of p53 and AP1 via the ataxia telangiectasia mutated (ATM)- and c-Jun N-terminal kinase (JNK)-signaling pathways activated by DSBs. Thus, BLM-s is likely an apoptosis sensor activated by DSBs accumulating in postmitotic immature neurons.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2211124714007268; http://dx.doi.org/10.1016/j.celrep.2014.08.050; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84907983655&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/25263558; https://linkinghub.elsevier.com/retrieve/pii/S2211124714007268; https://dx.doi.org/10.1016/j.celrep.2014.08.050
Elsevier BV
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