Ask about this productRelated genes to: PPP2R1A antibody
- Gene:
- PPP2R1A NIH gene
- Name:
- protein phosphatase 2 scaffold subunit Aalpha
- Previous symbol:
- -
- Synonyms:
- PR65A, PP2A-Aalpha, PP2AA
- Chromosome:
- 19q13.41
- Locus Type:
- gene with protein product
- Date approved:
- 1993-01-25
- Date modifiied:
- 2018-07-18
Related products to: PPP2R1A antibody
Related articles to: PPP2R1A antibody
- Although inhalation of nanoplastics (NPs) is widely recognized as a trigger of pulmonary injury, the mechanisms underlying lung damage induced by orally ingested NPs remain largely uncharacterized. Computational toxicology profiling predicted the involvement of efferocytosis in nanoplastic toxicity. Protein phosphatase 2A (PP2A) is an important regulator of macrophage function, and PP2A Aα deficiency impaired efferocytosis. To delineate the contribution of efferocytosis to nanoplastics-induced pulmonary toxicity, myeloid-specific PP2A Aα-deficient (HO) mice model (Ppp2r1a gene deletion) and matched wild-type (WT) littermates were administrated with polystyrene nanoplastics (PS-NPs) by gavage at dose of 10 mg/kg·bw for 4 successive weeks. PS-NPs treatment led to sex-dependent lung inflammation, oxidative damage, and apoptosis in WT mice, which were further aggravated in HO mice. Proteomics analysis revealed impaired efferocytosis in HO mice was associated with perturbations in protein kinase A, ERK/MAPK, Hedgehog signaling pathway etc. In vitro studies confirmed that PP2A Aα deficiency dysregulated Hedgehog signaling, thereby suppressing macrophage efferocytosis and exacerbating pulmonary injury following PS-NPs exposure. Notably, we identified biochanin A as a compound capable of attenuating PS-NPs-induced pulmonary inflammation by enhancing efferocytosis. Together, these findings uncover a novel PP2A-Hedgehog-efferocytosis axis in NPs-induced pulmonary injury and highlight biochanin A as a potential intervention candidate for particulate pollutants-associated respiratory diseases. - Source: PubMed
Publication date: 2026/05/20
Zhang JiaxinZhang YuweiWen LixianLi ZiyanCai YuluWan MengtingLi WenxueZhu XiaonianPang YaqinLi DaochuanChen ShenGuo PingWang QingChen WenChen Liping - Protein Phosphatase 2 A (PP2A), a key tumor suppressor, is frequently inactivated in cancer through mutations in its scaffold-encoding gene, . This is particularly common in aggressive gynecologic malignancies, specifically uterine serous carcinoma (USC) and ovarian clear cell carcinoma (OCCC). A compelling paradox has emerged: while these mutations are potent oncogenic drivers, they are also powerful predictive biomarkers for an exceptional response to immune checkpoint inhibitor (ICI) therapy. - Source: PubMed
Publication date: 2026/04/30
Chen JunyingTan YudiWei YuyingJin YuxuanHuang Jingwen - Myocardial fibrosis, characterized by excessive collagen deposition and fibroblast activation, is a pivotal pathological process driving heart failure after myocardial infarction (MI). Our prior research revealed that Brahma-related gene 1 (BRG1) expression is elevated after MI and exacerbated cardiac electrophysiological remodeling; however, its precise role and molecular mechanism in post-MI fibrosis remain undefined. - Source: PubMed
Publication date: 2026/03/16
Cui YunfengJin JingCui YingtaoMa ZiyueTong TingtingXiong LisiShen MeimeiZhao YuGuo XinLiang WenZhao HongxiaBan TaoHuo Rong - BACKGROUND: Sodium overload-induced cell death is a novel mode of cell death that differs from other modes and is a very promising new target for cancer therapy. In addition, sodium overload-induced cell death plays a crucial role in cancer progression and patient prognosis. Therefore, our study aims to establish a survival prediction model for patients with lung adenocarcinoma (LUAD) based on related genes, exploring the immune landscape and providing new insights for future individualized treatment protocols. METHOD: We analyzed the expression and clinical significance of TRPM4-related genes in LUAD using data from TCGA and GEO databases. We used transcriptomics, immune infiltration assays, and spatial transcriptomics (ST). Kaplan-Meier survival analysis was used to assess the relationship between TRPM4-related genes and prognosis. Enrichment analyses identified biological processes and pathways associated with TRPM4 and also assessed its relationship with the immune microenvironment and drug sensitivity. RESULTS: We identified 19 oncogenic driver genes and modeled proportional hazard regression. The results showed that the survival rate of the high-risk group was significantly reduced in both the training and testing sets. Additionally, the high-risk group exhibited lower levels of immune cell infiltration and immune checkpoint expression compared to the low-risk group. Based on 19 genes, LMNA, PPP2R1A, and PDXK were identified as key genes by single-cell sequencing and spatial transcriptome sequencing. - Source: PubMed
Publication date: 2026/03/17
Yu Wei-JieMiao Zhou-LinAiniwaer Julaiti - Recent studies have indicated that phosphoethanolamine cytidylyltransferase 2 (PCYT2) is aberrantly expressed in various tumors, influencing tumor progression, metastasis, and drug resistance. However, the role of PCYT2 in clear cell renal cell carcinoma (ccRCC) remains unexplored. The objective of this research is to explore the expression changes of PCYT2 in ccRCC and elucidate its potential regulatory effects on ccRCC biological functions, alongside the underlying molecular mechanisms. Through sequencing data analysis and clinical tissue assessments, we discovered a notable downregulation of PCYT2 in ccRCC tissues, with lower PCYT2 expression correlating with poorer patient prognosis. Gene overexpression and silencing experiments demonstrated that PCYT2 overexpression exerted notable anti-cancer effects, including inhibition of cell proliferation, migration, and invasion. Silencing PCYT2 produced opposite effects, which could be reversed by PCYT2 overexpression. Mechanistic studies revealed that PCYT2 promoted the phosphorylation of Yes-associated protein 1 (YAP1), preventing its nuclear translocation and thereby inhibiting YAP1 pathway activation. Further investigations indicated that the regulatory effect of PCYT2 on YAP1 phosphorylation was dependent on PPP2R1A. In vivo studies corroborated these findings, showing that PCYT2 overexpression significantly restrained tumor formation, accompanied by downregulation of the YAP1 pathway. Our findings offer substantial evidence that PCYT2 acts as a tumor suppressor in ccRCC, with its mechanism linked to the regulation of YAP1 pathway activation. This study offers fresh perspectives on the molecular pathogenesis of ccRCC and identifies PCYT2 as a potential candidate for therapeutic strategies in this disease. - Source: PubMed
Publication date: 2026/03/07
Nan NingGuo HaoHuang YanChen JuanQiang Xiaolong