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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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-kB-dependent Signaling Pathway02:26

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...
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...
Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

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NF-&#954;B-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
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NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

Neuronal RING finger protein 11 (RNF11) regulates canonical NF-κB signaling.

Elaine L Pranski1, Nirjari V Dalal, Jeremy H Herskowitz

  • 1Center for Neurodegenerative Disease, Department of Neurology, Emory University School of Medicine, 615 Michael St,, Suite 500, Atlanta, GA 30322, USA. epransk@emory.edu

Journal of Neuroinflammation
|April 18, 2012
PubMed
Summary
This summary is machine-generated.

RING finger protein 11 (RNF11) negatively regulates neuronal NF-κB signaling. Loss of RNF11 function in neurons may exacerbate inflammatory responses, impacting neurodegenerative disease progression.

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A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

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NF-&#954;B-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
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A Guide to Production, Crystallization, and Structure Determination of Human IKK1/&#945;
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A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • RING finger protein 11 (RNF11) is expressed in neurons and associated with Lewy bodies in Parkinson's disease.
  • The NF-κB pathway is crucial for nervous system development and function, with dysregulation linked to neuroinflammation and neurodegeneration.

Purpose of the Study:

  • To investigate the role of RNF11 in regulating canonical NF-κB signaling in neurons.
  • To understand the implications of RNF11 function in neuroinflammation and neurodegenerative diseases.

Main Methods:

  • Short hairpin RNA (shRNA)-mediated knockdown of RNF11 in human neuroblastoma cells and murine primary neurons.
  • Luciferase assays to measure NF-κB activity.
  • Coimmunoprecipitation and site-directed mutagenesis to analyze protein interactions and functional domains.

Main Results:

  • RNF11 acts as a negative regulator of canonical neuronal NF-κB signaling.
  • RNF11 interacts with the A20 ubiquitin-editing protein complex in neurons.
  • RNF11 depletion leads to increased levels of inflammatory markers (MCP-1, TNF-α) in neurons.

Conclusions:

  • RNF11 negatively regulates NF-κB signaling in the nervous system.
  • Compromised RNF11 function may lead to exaggerated inflammatory responses, potentially contributing to neurodegenerative disease pathogenesis.