Tlr4 Nf-κb Signaling
Tlr4 Nf-κb Signaling - 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...
04:08
An Assay for TLR-Dependent NF-кB/AP-1 Transcription Factor Signaling in Macrophages
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2025
This video demonstrates an assay to examine the toll-like receptor(TLR)-dependent activity of the transcription factors nuclear factor-kappa-B (NF-κB) and activator protein-1 (AP-1) in macrophages. The TLRs trigger a pro-inflammatory signaling cascade upon recognizing damage-associated molecular patterns (DAMPs), activating NF-κB and AP-1. The engineered reporter macrophages produce secreted embryonic alkaline phosphatase (SEAP) enzyme upon NF-κB and AP-1 activation, which is detected via a...
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.
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.
01:26
Signal and System
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2024
A signal x(t) is a set of data or a time function representing a variable of interest. Signals typically convey information about a phenomenon, such as atmospheric temperature, humidity, human voice, television images, a dog's bark, or birdsongs. More generally, a signal can be a function of more than one independent variable. For instance, images depend on horizontal and vertical positions and can be regarded as two-dimensional signals. However, this text will focus on one-dimensional signals...
FAQs
MyD88 and TRIF connect activated TLR4 to downstream signaling, but they represent separate adaptor components within the pathway. Their involvement links receptor detection to kinase activity involving IRAK, TRAF6, and TAK1. Examining these adaptor-dependent steps helps investigators determine how an external danger signal is translated into the intracellular events that ultimately regulate inflammatory gene expression.
The kinase cascade functions as an ordered relay rather than as an isolated reaction. IRAK, TRAF6, and TAK1 participate downstream of the adaptor proteins, leading to stimulation of the IKK complex. This sequence matters because IKK activity controls IκB degradation, creating the molecular link between receptor engagement and NF-κB activation.
Once IKK is stimulated, degradation of IκB removes a barrier to NF-κB activity. NF-κB can then move into the nucleus, where it promotes transcription of cytokines, chemokines, and other immune mediators. This step is the pathway’s principal connection to changes in gene expression, so nuclear NF-κB activity provides a useful focus for understanding inflammatory responses.
TLR4-NF-κB signaling is relevant to both microbial infection and tissue-associated disease because the initiating danger signal may come from lipopolysaccharide or tissue-derived sources. This distinction broadens the pathway’s medical importance beyond infection alone. It helps explain why the same inflammatory signaling framework is considered in studies of immunity, chronic inflammation, and disease.
Medical research applies this pathway to conditions in which inflammation is important to disease processes. The overview specifically identifies sepsis, chronic inflammation, and autoimmune disorders as relevant settings. In these contexts, researchers can relate receptor-proximal events and NF-κB-driven inflammatory gene expression to broader disease mechanisms, helping frame questions about immune dysregulation and therapeutic intervention.
Potential anti-inflammatory therapies are one reason to map each signaling step from TLR4 through NF-κB. The adaptor proteins, kinase cascade, IKK complex, IκB, and nuclear transcriptional response represent connected points for studying how inflammatory mediator production might be altered. This mechanistic view supports research into therapies intended to influence inflammation in infection, immunity, and disease.