PPP2R3A antibody
- Known as:
- PPP2R3A (anti-)
- Catalog number:
- orb100650
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- PPP2R3A antibody
Related genes to: PPP2R3A antibody
- Gene:
- PPP2R3A NIH gene
- Name:
- protein phosphatase 2 regulatory subunit B''alpha
- Previous symbol:
- PPP2R3
- Synonyms:
- PR130, PR72
- Chromosome:
- 3q22.2-q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-01-25
- Date modifiied:
- 2018-02-13
Related products to: PPP2R3A antibody
Related articles to: PPP2R3A antibody
- This study aimed to identify candidate genes and genetic markers affecting milk production traits in dual-purpose cattle, providing a foundation of data for marker-assisted breeding. Cis-eQTL analysis was performed on 83 Xinjiang brown cattle and 80 Chinese Simmental cattle using whole-genome resequencing and RNA-seq data derived from blood samples. Candidate genes were prioritized by overlapping the eGenes with genes from previous selective signature analyses. In Xinjiang brown cattle, 293,758 cis-eQTLs regulating 1,720 genes were identified, whereas 78,735 cis-eQTLs regulating 569 genes were found in Chinese Simmental cattle. By overlapping the eGenes with candidate genes from previous selective signature analyses, we prioritized 103 genes (e.g., , and ) in Xinjiang brown cattle and 26 candidate genes (e.g., and ) in Chinese Simmental cattle as potentially related to milk production traits. These results provide valuable data for the development of new dairy lines in Xinjiang brown cattle and for future genomic selection in dairy-oriented Chinese Simmental cattle. - Source: PubMed
Publication date: 2026/07/21
Ma KailunLi XueZhang MenghuaWang DanMa ShengchaoHuang XixiaChen QiumingXu Lei - Herpes simplex virus type-1 (HSV-1) affects over 60% of the human population and increasingly develops resistance to antiviral therapies. Efficient HSV-1 replication requires host-derived deoxynucleotide triphosphates and the manipulation of cellular DNA replication and repair. This work positions the protein phosphatase 2A (PP2A) regulatory subunit PR130 (PPP2R3A) as cellular factor that suppresses the replication of laboratory strains and clinical isolates of HSV-1 in epithelial and neuronal cells. HSV-1 infection in turn decreases PR130 levels. Global proteome and phosphoproteome profiling combined with functional assays demonstrate that PR130 modulates key regulators of the cell cycle and DNA repair. PR130 controls the expression and phosphorylation of the cyclin-dependent kinase (CDK) inhibitor p21 (CDKN1A) at serine 130 (S130) which CDK2 catalyzes. The levels and activities of p21, which HSV-1 infection attenuates, and CDK2 are decisive factors for HSV-1 replication. Inhibition of the ubiquitin-specific protease USP7 stabilizes the p53-p21 axis and reduces HSV-1 viral titers. Additionally, PR130 depletion enhances signaling of the DNA damage-responsive checkpoint kinase ataxia-telangiectasia mutated (ATM) upon HSV-1 infection and creates a dependency of HSV-1 replication on ATM activity. These findings uncover host-intrinsic mechanisms regulating HSV-1 replication and highlight PR130 as central hub regulator of HSV-1 infection. - Source: PubMed
Publication date: 2026/05/15
Jungwirth JohannesJacob Christoph FNguyen AlexandraBeyer MandyMieland Andreas ODejung MarioChen Jia-XuanBrenner WalburgisEhrhardt ChristinaHenke AndreasKrämer Oliver H - Common regulatory and coding variants may influence type 2 diabetes (T2D) risk by altering gene regulation or protein function. Identifying these variants and their associations with disease risk may inform disease control strategies. This study prioritized candidate variants by integrating two-group comparative genotyping with in-silico structural and dynamic analyses. - Source: PubMed
Publication date: 2026/05/06
Rezaei Seyyed Amin SeyyedKohkalani MoeinMehri MaghsoudDerakhshan Sima MansooriZanchi Fernando BertonCaceres Rafael AndradeAmirfiroozi Akbar - BACKGROUND: PPP2R3A is a key regulatory subunit of the PP2A B’’ family that encodes PR130 and PR72, two isoforms highly expressed in the heart. It has been implicated in heart failure and represents a potential molecular hub connecting pathological remodeling to disease progression. However, its functional dynamics in pressure overload-induced heart failure remain unclear. This study aims to investigate the expression changes and regulatory mechanisms of PPP2R3A in pressure overload-induced decompensated heart failure. METHODS: A chronic pressure overload model was established in C57BL/6J mice using transverse aortic constriction (TAC), and cardiac function and remodeling were assessed by echocardiography and histological analyses. In vitro, PPP2R3A was silenced or overexpressed in H9c2 cardiomyocytes to evaluate its effects on transcription, viability, and apoptosis. Protein interactions and downstream signaling were examined using co-immunoprecipitation, GST pull-down, and Western blotting. RESULTS: PPP2R3A expression was markedly downregulated in the TAC model, accompanied by impaired systolic function, pathological hypertrophy, and fibrosis. In cardiomyocytes, PPP2R3A knockdown exacerbated apoptosis and reduced viability, whereas overexpression promoted robust survival. Mechanistically, PPP2R3A stabilized the β-catenin destruction complex, thereby suppressing canonical Wnt/β-catenin signaling and preventing maladaptive β-catenin-driven transcription. Proteomic assays identified a direct interaction between PPP2R3A and RGS19, with PPP2R3A negatively regulating RGS19 protein abundance and Ser/Thr phosphorylation. CONCLUSIONS: PPP2R3A protects the heart against pressure overload-induced heart failure by stabilizing the β-catenin degradation complex and limiting maladaptive Wnt/β-catenin signaling. Its regulation of RGS19 reveals a novel axis in the transition from compensated to decompensated heart failure, highlighting PPP2R3A as a potential therapeutic target. - Source: PubMed
Publication date: 2026/04/22
Qin ShuangSu LinggeGao JingWu ChunyanZhang YatingShi HongqiongSong Guibo - Crohn disease (CD) is a chronic, recurrent inflammatory bowel disease. Mesenchymal stem cell-derived exosomes (MSC-Exos) have emerged as promising cell-free treatments for CD. - Source: PubMed
Feng TingQiu YunChen BailiHuang XuanzhiFeng RuiHe YaoZeng ZhirongChen MinhuZhang Shenghong