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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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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NF-kB-dependent Signaling Pathway02:26

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Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
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Spatial and temporal information coding and noise in the NF-κB system.

Marco Marcello1, Michael R H White

  • 1School of Biological Sciences, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK. M.Marcello@liverpool.ac.uk

Biochemical Society Transactions
|September 25, 2010
PubMed
Summary
This summary is machine-generated.

Pulsatile inflammatory signals, like tumor necrosis factor alpha (TNFα), trigger nuclear factor-kappa B (NF-κB) oscillations. The frequency of these signals affects NF-κB translocation amplitude and gene expression, impacting cellular responses.

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Area of Science:

  • Cellular biology
  • Immunology
  • Systems biology

Background:

  • Nuclear factor-kappa B (NF-κB) is crucial for cellular stress and immune responses.
  • NF-κB activation leads to dynamic oscillations in its nuclear abundance.
  • Pulsatile inflammatory signals are common in biological systems.

Purpose of the Study:

  • To investigate the impact of pulsatile tumor necrosis factor alpha (TNFα) stimulation intervals on NF-κB nuclear translocation dynamics.
  • To explore the role of negative feedback loops in regulating NF-κB oscillations and cellular heterogeneity.
  • To understand the functional significance of NF-κB oscillation frequency in gene expression patterns.

Main Methods:

  • Cells were treated with repeated short pulses of TNFα at various intervals.
  • Observed NF-κB nuclear translocation patterns using microscopy.
  • Developed deterministic and stochastic mathematical models to simulate system dynamics.
  • Analyzed NF-κB-dependent gene expression in response to different stimulation frequencies.

Main Results:

  • Synchronous NF-κB nuclear translocation cycles were observed across all analyzed pulse intervals.
  • Lower frequency TNFα stimulation resulted in full-amplitude translocations, while higher frequencies led to reduced amplitudes.
  • Mathematical models predicted negative feedback loops influencing system resetting and cellular heterogeneity.
  • Varying stimulation intervals altered NF-κB-dependent gene expression patterns, highlighting the functional role of oscillation frequency.

Conclusions:

  • The frequency of pulsatile inflammatory signals significantly modulates NF-κB dynamics and downstream gene expression.
  • Negative feedback mechanisms are critical for regulating NF-κB resetting and managing cellular heterogeneity.
  • NF-κB oscillations play a functional role in cellular decision-making, contributing to biological complexity and robustness.