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NF-kappaB dimers in the regulation of neuronal survival.
Int Rev Neurobiol. 2009; 85:351-62.IR

Abstract

Nuclear factor-kappaB (NF-kappaB) is a dimeric transcription factor composed of five members, p50, RelA/p65, c-Rel, RelB, and p52 that can diversely combine to form the active transcriptional dimer. NF-kappaB controls the expression of genes that regulate a broad range of biological processes in the central nervous system such as synaptic plasticity, neurogenesis, and differentiation. Although NF-kappaB is essential for neuron survival and its activation may protect neurons against oxidative-stresses or ischemia-induced neurodegeneration, NF-kappaB activation can contribute to inflammatory reactions and apoptotic cell death after brain injury and stroke. It was proposed that the death or survival of neurons might depend on the cell type and the timing of NF-kappaB activation. We here discuss recent evidence suggesting that within the same neuronal cell, activation of diverse NF-kappaB dimers drives opposite effects on neuronal survival. Unbalanced activation of NF-kappaB p50/RelA dimer over c-Rel-containing complexes contributes to cell death secondary to the ischemic insult. While p50/RelA acts as transcriptional inducer of Bcl-2 family proapoptotic Bim and Noxa genes, c-Rel dimers specifically promote transcription of antiapototic Bcl-xL gene. Changes in the nuclear content of c-Rel dimers strongly affect the threshold of neuron vulnerability to ischemic insult and agents, likewise leptin, activating a NF-kappaB/c-Rel-dependent transcription elicit neuroprotection in animal models of brain ischemia.

Authors+Show Affiliations

Division of Pharmacology and Experimental Therapeutics, Department of Biomedical Sciences and Biotechnologies, School of Medicine, University of Brescia, Brescia 25123, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

19607980

Citation

Sarnico, Ilenia, et al. "NF-kappaB Dimers in the Regulation of Neuronal Survival." International Review of Neurobiology, vol. 85, 2009, pp. 351-62.
Sarnico I, Lanzillotta A, Benarese M, et al. NF-kappaB dimers in the regulation of neuronal survival. Int Rev Neurobiol. 2009;85:351-62.
Sarnico, I., Lanzillotta, A., Benarese, M., Alghisi, M., Baiguera, C., Battistin, L., Spano, P., & Pizzi, M. (2009). NF-kappaB dimers in the regulation of neuronal survival. International Review of Neurobiology, 85, 351-62. https://doi.org/10.1016/S0074-7742(09)85024-1
Sarnico I, et al. NF-kappaB Dimers in the Regulation of Neuronal Survival. Int Rev Neurobiol. 2009;85:351-62. PubMed PMID: 19607980.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - NF-kappaB dimers in the regulation of neuronal survival. AU - Sarnico,Ilenia, AU - Lanzillotta,Annamaria, AU - Benarese,Marina, AU - Alghisi,Manuela, AU - Baiguera,Cristina, AU - Battistin,Leontino, AU - Spano,Pierfranco, AU - Pizzi,Marina, PY - 2009/7/18/entrez PY - 2009/7/18/pubmed PY - 2009/9/11/medline SP - 351 EP - 62 JF - International review of neurobiology JO - Int Rev Neurobiol VL - 85 N2 - Nuclear factor-kappaB (NF-kappaB) is a dimeric transcription factor composed of five members, p50, RelA/p65, c-Rel, RelB, and p52 that can diversely combine to form the active transcriptional dimer. NF-kappaB controls the expression of genes that regulate a broad range of biological processes in the central nervous system such as synaptic plasticity, neurogenesis, and differentiation. Although NF-kappaB is essential for neuron survival and its activation may protect neurons against oxidative-stresses or ischemia-induced neurodegeneration, NF-kappaB activation can contribute to inflammatory reactions and apoptotic cell death after brain injury and stroke. It was proposed that the death or survival of neurons might depend on the cell type and the timing of NF-kappaB activation. We here discuss recent evidence suggesting that within the same neuronal cell, activation of diverse NF-kappaB dimers drives opposite effects on neuronal survival. Unbalanced activation of NF-kappaB p50/RelA dimer over c-Rel-containing complexes contributes to cell death secondary to the ischemic insult. While p50/RelA acts as transcriptional inducer of Bcl-2 family proapoptotic Bim and Noxa genes, c-Rel dimers specifically promote transcription of antiapototic Bcl-xL gene. Changes in the nuclear content of c-Rel dimers strongly affect the threshold of neuron vulnerability to ischemic insult and agents, likewise leptin, activating a NF-kappaB/c-Rel-dependent transcription elicit neuroprotection in animal models of brain ischemia. SN - 0074-7742 UR - https://www.unboundmedicine.com/medline/citation/19607980/NF_kappaB_dimers_in_the_regulation_of_neuronal_survival_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0074-7742(09)85024-1 DB - PRIME DP - Unbound Medicine ER -