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Related Experiment Video

Updated: Jul 9, 2026

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Published on: September 20, 2024

p38alpha stabilizes interleukin-6 mRNA via multiple AU-rich elements.

Wenpu Zhao¹, Min Liu, Keith L Kirkwood

¹Department of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, Michigan 48109-1078, USA.

The Journal of Biological Chemistry

|November 29, 2007

Summary

p38alpha signaling is crucial for interleukin-6 (IL-6) biosynthesis by stabilizing IL-6 mRNA. Specific AU-rich elements (AREs) in the IL-6 3'-untranslated region (UTR) are targeted by p38alpha, influencing mRNA stability and translation.

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Last Updated: Jul 9, 2026

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Published on: September 20, 2024

Area of Science:

Molecular Biology
Cell Signaling
Gene Regulation

Background:

AU-rich elements (AREs) in 3 -untranslated regions (UTRs) of mRNA regulate mRNA degradation and translation.
p38alpha MAPK signaling is essential for post-transcriptional control of pro-inflammatory cytokines.

Purpose of the Study:

To identify cis-acting elements in interleukin-6 (IL-6) 3 -UTR mRNA regulated by p38alpha signaling.
To elucidate the mechanism by which p38alpha signaling affects IL-6 mRNA stability and translation.

Main Methods:

Utilized mouse embryonic fibroblasts (MEFs) from p38alpha(+/+) and p38alpha(-/-) mice.
Employed 3 -UTR truncation and AUUUA motif mutation in a gene reporter system.
Performed RNA secondary structure analysis.

Main Results:

p38alpha is essential for IL-1-induced IL-6 biosynthesis.
p38alpha promotes IL-6 mRNA stability through its 3 -UTR.
ARE1, ARE2, and ARE5 within the IL-6 3 -UTR are targeted by p38alpha.
The IL-6 3 -UTR region (56-173) is critical for p38alpha-mediated mRNA stabilization.

Conclusions:

p38alpha signaling directly targets specific AREs in the IL-6 3 -UTR to control mRNA stability and translation.
The findings reveal a key mechanism for regulating IL-6 expression at the post-transcriptional level.