Related Experiment Video

Updated: Jul 7, 2026

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH
07:54

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH

Published on: August 19, 2014

Disruption of ZAS3 in mice alters NF-kappaB and AP-1 DNA binding and T-cell development

Carl E Allen1, John Richards, Natarajan Muthusamy

  • 1Department of Pediatrics and Center for Cell and Developmental Biology, Columbus Children's Research Institute, Columbus, OH 43205, USA.

Gene Expression
|February 9, 2008
PubMed

Insights

Zinc finger protein ZAS3 plays a subtle role in T-cell development and activation. Its absence in mice alters gene expression and immune cell populations, impacting T-cell signaling pathways.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Large zinc finger proteins (ZAS) regulate gene transcription and signal transduction pathways (TGF-beta, TNF-alpha).
  • Endogenous ZAS3 protein is rapidly degraded in lymphocytes, hindering in vitro functional studies.
  • Understanding ZAS3's physiological role is crucial for comprehending immune system regulation.

Purpose of the Study:

  • To investigate the in vivo physiological function of ZAS3.
  • To analyze the impact of ZAS3 deficiency on gene expression and immune cell development.

Main Methods:

  • Generation of ZAS3-deficient (ZAS3-/-) mice.
  • Oligonucleotide-based microarray analysis of thymic gene expression.
  • Gel mobility shift assays to assess DNA binding activities.
  • Flow cytometry for lymphocyte subset analysis.

Main Results:

  • ZAS3 deficiency caused subtle but consistent differences in gene expression in the thymus, particularly in genes related to receptor and signal transduction.
  • Altered DNA binding activities of NF-kappaB and AP-1 were observed in ZAS3-deficient tissues.
  • ZAS3 deficiency led to a decreased CD4/CD8 ratio and reduced CD69 expression in thymocytes.
  • An increased number of memory T cells was found in peripheral CD4+ ZAS3-/- lymphocytes.

Conclusions:

  • ZAS3 has a subtle but broad function in regulating T-cell development and activation.
  • ZAS3 deficiency impacts immune cell signaling and T-cell subset composition.
  • ZAS3-deficient mice serve as a valuable model for studying ZAS3's role in the immune system.

More Related Videos

Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis14:58

Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis

Published on: February 13, 2014

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders07:43

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

Published on: May 12, 2015

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...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...