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IGF2BP2 condensates stabilize DOK3 to negatively regulate inflammatory responses.

Jian Chen1, Weixin Chen1, Xiaojing Shan2

  • 1Key Laboratory of Stem Cells and Tissue Engineering, Zhongshan School of Medicine, Sun Yat-sen University, Ministry of Education, Guangzhou, China.

Journal of Immunology (Baltimore, Md. : 1950)
|April 18, 2026
PubMed
Summary
This summary is machine-generated.

Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) regulates inflammation by forming condensates that stabilize DOK3 mRNA. Loss of IGF2BP2 boosts pro-inflammatory cytokine production, while its presence dampens immune responses.

Keywords:
IGF2BP2biomolecular condensatesimmune regulationinflammationm6A modification

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Area of Science:

  • Immunology
  • Molecular Biology
  • RNA Biology

Background:

  • Negative immune regulators are vital for homeostasis, but their mechanisms require further elucidation.
  • RNA-binding proteins play critical roles in post-transcriptional gene regulation.

Purpose of the Study:

  • To investigate the role of IGF2BP2 as a negative regulator of bacterial-induced inflammation.
  • To elucidate the molecular mechanisms underlying IGF2BP2's function in immune homeostasis.

Main Methods:

  • Investigated IGF2BP2's role in phase-separated condensate formation with G3BP1.
  • Assessed pro-inflammatory cytokine production (IL-6, TNF-α, IL-1β) in the presence or absence of IGF2BP2.
  • Analyzed NF-κB signaling pathway activation and DOK3 mRNA expression.
  • Identified m6A modifications on DOK3 mRNA using sequencing.

Main Results:

  • IGF2BP2 acts as a negative regulator of bacterial-induced inflammation, forming G3BP1-dependent condensates.
  • IGF2BP2 deficiency amplifies pro-inflammatory cytokine production and enhances NF-κB signaling via reduced DOK3 expression.
  • Restoring DOK3 expression mitigates the hyper-inflammatory phenotype in IGF2BP2-deficient cells.
  • m6A modifications at specific sites on DOK3 mRNA facilitate IGF2BP2 binding and stabilization.

Conclusions:

  • IGF2BP2 modulates immune responses through m6A-dependent stabilization of DOK3 mRNA.
  • This study reveals a novel mechanism of immune regulation by IGF2BP2, impacting inflammatory disease therapeutics.