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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
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Hypoxia Induced NF-κB.

Laura D'Ignazio1, Sonia Rocha2

  • 1Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dow street, Dundee DD1 5EH, UK. l.dignazio@dundee.ac.uk.

Cells
|March 24, 2016
PubMed
Summary
This summary is machine-generated.

Hypoxia activates Nuclear Factor-κB (NF-κB), a key stress response factor. This review details the molecular mechanisms and NF-κB

Keywords:
FIHHIF-1HypoxiaIKKNF-κBPHDsTAKubiquitin

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Physiology

Background:

  • Nuclear Factor-κB (NF-κB) is a critical transcription factor involved in cellular stress responses.
  • Hypoxia, characterized by decreased oxygen availability, is a significant cellular stressor.
  • The precise mechanisms by which hypoxia activates NF-κB are not fully elucidated.

Purpose of the Study:

  • To review and synthesize current findings on the molecular mechanisms of hypoxia-induced NF-κB activation.
  • To identify key molecules involved in the hypoxia-mediated NF-κB signaling pathway.
  • To discuss the functional role of NF-κB in the cellular response to hypoxic conditions.

Main Methods:

  • Literature review of peer-reviewed scientific articles.
  • Analysis of experimental data from studies investigating hypoxia and NF-κB signaling.
  • Synthesis of findings from various molecular and cellular biology research.

Main Results:

  • Several molecular pathways have been implicated in hypoxia-induced NF-κB activation.
  • Specific molecules and signaling cascades have been identified as crucial mediators.
  • NF-κB plays a significant role in regulating gene expression and cellular adaptation to low oxygen.

Conclusions:

  • The activation of NF-κB by hypoxia is a complex process involving multiple molecular players.
  • Understanding these mechanisms is crucial for comprehending cellular responses to stress.
  • Further research is warranted to fully elucidate the intricacies of this pathway and its therapeutic implications.