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
- 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 - - 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 - Necroptosis, a form of programmed inflammatory cell death, plays a crucial role in tumor development, necrosis, metastasis, and immune response. This study aimed to explore the role of necroptosis in BLCA and construct a new prognostic model to guide clinical treatment and predict individualized treatment response. - Source: PubMed
Publication date: 2024/11/25
Yao DongnuanYu WeitaoMa XuemingTian Junqiang