Nf-kappa B
Nf-kappa B - Related Videos
02:26
NF-κB-dependent Signaling Pathway
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2021
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. NF-κB-dependent Signaling Mechanism The heterodimer of NF-κB...
14:58
Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
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Cited by 1 •
2014
Methods for the manipulation and analysis of NF-κB-dependent adult hippocampal neurogenesis are described. A detailed protocol is presented for a dentate gyrus-dependent behavioral test (termed the spatial pattern separation-Barnes maze) for the investigation of cognitive outcome in mice. This technique should also help enable investigations in other experimental settings.
08:51
Intraductal Injection of LPS as a Mouse Model of Mastitis: Signaling Visualized via an NF-κB Reporter Transgenic
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Cited by 14 •
2012
Described here is a technique in which lipopolysaccharide is injected into the lactating mouse mammary gland via the nipple to simulate mastitis, a condition commonly caused by bacterial infection. Lipopolysaccharide injection results in increased nuclear factor kappa B (NF-κB) signaling, visualized through bioluminescent imaging of an NF-κB luciferase reporter mouse.
10:57
NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
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Cited by 4 •
2020
Here, we present a protocol to quickly and easily measure nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation in cell lines expressing NF-κB::luciferase reporter constructs, via measurements of luminescence in the cell lysate. Additionally, gene expression is determined via RT-qPCR isolated from cells infected with Salmonella Typhimurium.
03:28
A Permeable Membrane Insert-Based Infection System to Study the Impact of Bacterial Toxins
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2025
This video demonstrates a permeable membrane insert-based infection system to assess the impact of secreted bacterial toxins. By eliminating direct contact between the bacterial pathogen and the host cells using a permeable membrane, this technique allows for studying the effect of toxins secreted by pathogenic bacteria on mammalian host cells.
FAQs
IκB proteins provide a resting-state checkpoint by retaining Nf-kappa B in the cytoplasm. When an appropriate immune, stress, or cellular signal activates IκB kinase, the kinase promotes IκB degradation. This releases the transcription factor and permits its movement toward the nucleus, linking an external or intracellular signal to a potential change in gene expression.
Nuclear entry converts pathway activation into a transcriptional response. After leaving the cytoplasmic restraint imposed by IκB, Nf-kappa B can enter the nucleus, bind DNA, and influence transcription. This step matters because it connects signaling events with functional cellular outcomes, including inflammatory signaling, neuronal survival responses, glial activation, and reactions to neural injury.
The pathway can participate in several neural processes rather than producing one fixed response. Depending on the surrounding immune, stress, or cellular signals, its transcriptional activity may relate to inflammatory signaling, neuronal survival, glial activation, or injury responses. This context dependence makes the pathway useful for studying how neural cells respond to changing conditions.
A pathway-focused investigation can follow the sequence from cellular stimulation to IκB kinase activation, IκB degradation, Nf-kappa B release, nuclear entry, DNA binding, and altered transcription. Examining these linked events helps distinguish an upstream signaling change from a later gene-regulatory response and provides a framework for interpreting pathway activity in neural tissues.
Nf-kappa B studies help connect signaling activity with inflammatory gene regulation in neural tissues. Researchers can use the pathway as a framework for examining how immune or stress-related signals affect glial activation and other neural responses. This supports investigation of neuroinflammation as a cellular process associated with injury and neurological disease mechanisms.
Its relevance comes from the pathway's position between cellular signals and transcriptional changes linked to inflammation, neuronal survival, glial activation, and injury responses. Studying these relationships can clarify mechanisms associated with neurological disease and identify pathway events that may inform therapeutic strategies, without assuming that every activation state has the same effect.