Ppp2r5c, encoding the regulatory B56γ subunit of protein phosphatase 2A (PP2A), is crucial in various biological processes. PP2A is involved in cell proliferation, differentiation, transformation, and it influences the dephosphorylation of P53 at different residues. Alterations in Ppp2r5c expression pattern are associated with cell malignant transformation, making it potentially relevant in cancer research [5].

In multiple mouse models, Ppp2r5c shows significant impacts. In a COPD murine model, LincR-Ppp2r5c, a lncRNA affecting Ppp2r5c-related PP2A activity, regulates IL-1β ubiquitination in macrophages, promoting airway inflammation and emphysema; its deficiency ameliorates these symptoms [1]. In pulmonary cryptococcosis mouse model, LincR-Ppp2r5c deficiency enhances the fungicidal activity of neutrophils, reducing fungal burden and associated with increased IL-4 levels [2]. In a chronic allergic asthma mouse model, LincR-Ppp2r5c deficiency alleviates airway remodeling by inhibiting epithelial-mesenchymal transition through the PP2A/TGF-β1 signaling pathway [3]. Also, LincR-Ppp2r5c promotes Th2 cell differentiation through Ppp2r5c/PP2A by forming an RNA-DNA triplex in an acute asthma mouse model [4].

In conclusion, Ppp2r5c, via its role in PP2A, is involved in important biological processes and disease-related pathways. Gene knockout or deficiency models of Ppp2r5c in mice have revealed its significance in respiratory diseases such as COPD, pulmonary cryptococcosis, and allergic asthma, highlighting its potential as a therapeutic target in these disease areas.