Proteomics

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KAT8-mediated PCBP1 acetylation drives neutrophil recruitment in papain-induced airway inflammation

ABSTRACT: Emerging evidence implicates KAT8 as a critical modulator of inflammatory responses in lung diseases. Bosch et al. reported that MG149, a KAT8 inhibitor, reduces pro-inflammatory gene expression in lipopolysaccharide (LPS)-stimulated murine lung slices. Additionally, Liu et al. demonstrated that KAT8 promotes the cleavage and release of IL-33 through direct acetylation in airway epithelial cells in asthma models. However, KAT8 regulatory mechanism remains unexplored. To elucidate the molecular mechanism by which KAT8 modulates chemokine expression, we performed immunoprecipitation followed by mass spectrometry (IP-MS) to identify KAT8-interacting proteins. KEGG pathway enrichment analysis of the top 300 proteins with the highest coverage revealed significant enrichment in RNA binding and mRNA processing pathways, identifying these proteins as potential KAT8-interacting partners.

ORGANISM(S): Homo Sapiens

SUBMITTER: Ruina Huang  

PROVIDER: PXD078474 | iProX | Mon May 18 00:00:00 GMT+01:00 2026

REPOSITORIES: iProX

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KAT8-mediated PCBP1 acetylation drives neutrophil recruitment in papain-induced airway inflammation.

Huang Ruina R   Feng Zhihang Z   Zhang Wenchao W   Zhong Yu Y   Su Guomei G   Lai Xianwen X   Li Han H   Fang Zhenfu Z   Zhao Zhao Z   Zhang Mengting M   Li Shihai S   Yang Ruxing R   Gao Xiao X   Xiao Hongying H   Jiang Yang Y   Duan Jielin J   Lai Tianwen T  

American journal of respiratory cell and molecular biology 20260604

Macrophages play central role in driving airway inflammation during asthma pathogenesis, though the molecular mechanism governing their function remains incompletely understood. Here, we demonstrate that lysine acetyltransferase 8 (KAT8) plays a critical role in papain-induced neutrophilic airway inflammation through post-translational modification of poly(C)-binding protein 1 (PCBP1). We show that papain exposure significantly upregulates KAT8 expression in lung macrophages both in vivo and in  ...[more]

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