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Updated: May 25, 2026

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Published on: October 6, 2019

Does Δ133p53 isoform trigger inflammation and autoimmunity?

Hamish G Campbell¹, Tania L Slatter, Aaron Jeffs

¹Children's Medical Research Institute, University of Sydney, Sydney, NSW, Australia.

Cell Cycle (Georgetown, Tex.)

|January 21, 2012

Summary

The tumor suppressor p53 isoform, delta 133 p53 (Δ133p53), drives autoimmune disease development. Mice lacking Δ122p53 exhibit autoimmune symptoms and inflammation, linked to STAT1 pathway activation, a signature also seen in human lupus patients.

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

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Area of Science:

Immunology
Molecular Biology
Genetics

Background:

Autoimmune diseases involve the immune system attacking self- tissues, with unclear causes.
The tumor suppressor protein p53 has isoforms, including Δ133p53, whose roles in autoimmunity are unexplored.

Purpose of the Study:

To investigate the involvement of the p53 isoform Δ133p53 in the development of autoimmune diseases.

Main Methods:

Generated a mouse model (Δ122p53) lacking the Δ133p53 isoform.
Analyzed autoimmune/inflammation-like phenotypes, including autoantibodies and cytokine levels.
Utilized microarray analysis to identify gene expression changes and validated findings in human cells.

Main Results:

Δ122p53 mice developed autoantibodies, elevated pro-inflammatory cytokines, and lymphocyte aggregations.
Microarray analysis revealed Δ122p53 expression induced pro-inflammatory genes, including the STAT1 pathway and interferon-related profiles.
Identified similar genetic signatures in human systemic lupus erythematosus (SLE) patients and demonstrated Δ133p53 regulation of STAT1 in human cells.

Conclusions:

p53 isoforms, specifically Δ133p53, play a significant role in the development of autoimmune diseases.
The study establishes a novel link between p53 isoforms and autoimmunity, highlighting the STAT1 pathway as a key mediator.
Findings suggest potential therapeutic targets for autoimmune conditions by modulating p53 isoform activity.