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NF-κB-dependent Signaling Pathway

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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...

NF-kB-dependent Signaling Pathway

NF-kB-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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...

MAPK Signaling Cascades

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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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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NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

RNF11 modulates microglia activation through NF-κB signalling cascade.

Nirjari V Dalal¹, Elaine L Pranski, Malu G Tansey

¹Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA 30322, United States. nvdalal@emory.edu

Neuroscience Letters

|September 15, 2012

Summary

This summary is machine-generated.

RING finger protein 11 (RNF11) negatively regulates NF-κB signaling in microglia, crucial immune cells in the central nervous system. This finding highlights RNF11 as a potential therapeutic target for neurodegenerative diseases.

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Area of Science:

Neuroimmunology
Molecular Neuroscience

Background:

Microglia, the CNS immune cells, drive neuroinflammation in neurodegenerative diseases.
Sustained NF-κB pathway activation in microglia promotes chronic neuroinflammation.

Purpose of the Study:

To investigate the role of RING finger protein 11 (RNF11) in regulating NF-κB signaling in microglia.
To determine if RNF11 acts as a negative regulator of microglial inflammatory responses.

Main Methods:

Coimmunoprecipitation assays to confirm RNF11 and A20 complex formation in microglia.
Short hairpin RNA (shRNA) knockdown and overexpression of RNF11 to assess its impact on NF-κB activity.
Analysis of NF-κB target gene expression and cell viability assays.

Main Results:

RNF11 interacts with the A20 ubiquitin-editing complex in microglial cells.
RNF11 expression levels are inversely correlated with NF-κB pathway activation.
RNF11 overexpression protected microglial cells against lipopolysaccharide (LPS)-induced cytotoxicity.

Conclusions:

Microglial RNF11 functions as a key negative regulator of the NF-κB signaling pathway.
RNF11 represents a promising therapeutic target for modulating neuroinflammation in neurodegenerative conditions.