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Cited by 849

NF-kB: a crucial transcription factor for glial and neuronal cell function

O'Neill, L.A.J, Kaltschmidt, C.·1997·Trends in Neurosciences
DOI 10.1016/s0166-2236(96)01035-1
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Abstract

Transcription factors provide the link between early membrane-proximal signalling events and changes in gene expression. NF-kappa B is one of the best-characterized transcription factors. It is expressed ubiquitously and regulates the expression of many genes, most of which encode proteins that play an important and often determining role in the processes of immunity and inflammation. Apart from its role in these events, evidence has begun to accumulate that NF-kappa B is involved in brain function, particularly following injury and in neurodegenerative conditions such as Alzheimer's disease. NF-kappa B might also be important for viral replication in the CNS. An involvement of NF-kappa B in neuronal development is suggested from studies that demonstrate its activation in neurones in certain regions of the brain during neurogenesis. Brain-specific activators of NF-kappa B include glutamate (via both AMPA/KA and NMDA receptors) and neurotrophins, pointing to an involvement in synaptic plasticity. NF-kappa B can therefore be considered as one of the most important transcription factors characterized in brain to date and it might be as crucial for neuronal and glial cell function as it is for immune cells.

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  • Activation of NF-κB plays a pivotal role in the activation of astrocytes and their production of TNFα and other pro-inflammatory cytokines.

    “activation of NF-κB plays a pivotal role in the activation of astrocytes and their production of TNFα and other pro-inflammatory cytokines (O’Neill et al., 1997; Mattson et al., 2001).”

    From Evidence for miR‐181 involvement in neuroinflammatory responses of astrocytes (2013) · cites this paper as O’Neill et al., 1997

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Authors
O'Neill, L. A. J., & Kaltschmidt, C.
Venue
Trends in Neurosciences
Publisher
Elsevier BV
Published
1997-06
Volume
20
Issue
6
Pages
252-258
ISSN
0166-2236
DOI
10.1016/s0166-2236(96)01035-1
Cited by
849
References
2
Language
en
Licence
Funders
  • European Commission
  • Deutsche Forschungsgemeinschaft
  • Volkswagen Foundation

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