PPP2R2C polyclonal antibody
- Known as:
- PPP2R2C pab (anti-)
- Catalog number:
- PAB13658
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PPP2R2C polyclonal antibody
Related genes to: PPP2R2C polyclonal antibody
- Gene:
- PPP2R2C NIH gene
- Name:
- protein phosphatase 2 regulatory subunit Bgamma
- Previous symbol:
- -
- Synonyms:
- PR52, IMYPNO, MGC33570, PR55G, B55gamma
- Chromosome:
- 4p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-01-25
- Date modifiied:
- 2017-04-05
Related products to: PPP2R2C polyclonal antibody
Related articles to: PPP2R2C polyclonal antibody
- Renal cell carcinoma (RCC) is the most common malignancy of the urinary system, characterized by high incidence, mortality, and resistance to therapy. Its molecular heterogeneity presents challenges for effective precision treatment. RCC is highly heterogeneous, yet treatment guidelines rely predominantly on kidney renal clear cell carcinoma (KIRC) studies, neglecting other molecular subtypes, which limits therapy personalization for non-KIRC patients. This study aimed to explore the role of small ubiquitin-like modifier (SUMOylation)-associated genes in the progression and prognosis of RCC and its subtypes. We identified 298 SUMOylation-associated differentially expressed genes (DEGs), including 151 RCC-specific genes after excluding expression changes attributable to RCC subtype-specific variation. Ten core genes (, , , , , , , , , and ) were identified, with expression not only discriminates tumor from normal tissue but also separates KIRC from KICH/KIRP, proposing as a potential second-step biomarker for KIRC identification on top of traditional histology. Inter-subtype RCC heterogeneity represented a key factor limiting predictive performance of the six prognostic signature genes (, , , , and ). Its 5-year AUC exceeded 0.7 for every individual RCC subtype in the TCGA training cohort, with pooled 5-year AUCs of 0.61 (TCGA training cohort) and 0.67 (independent PCAWG validation cohort). The prognostic risk model demonstrated strong predictive performance, with a C-index of 0.791 before calibration and 0.774 after calibration. Importantly, the C-index remained above 0.75 throughout the 60-month follow-up period, indicating stable and robust long-term prognostic accuracy. High-risk patients exhibited greater immune cell infiltration, indicating potential for immunotherapy. Following secondary screening, three RCC cell lines (BFTC909, CAKI1, and CAL54) and five target genes (, , , and ) were identified as optimal candidates for subsequent mechanistic investigations. This study uncovers the prognostic and functional relevance of SUMOylation in RCC and offers a novel framework for biomarker development, therapeutic targeting, and immunotherapeutic stratification. - Source: PubMed
Publication date: 2026/07/23
Zhang XiaoboLi ZhimingLin RuoxinYang SupingSun XiaohuiChen Shicheng - Lung adenocarcinoma (LUAD) remains lethal primarily due to its tendency for early metastasis and the universal development of chemotherapy resistance. The results of this study delineate a coherent signaling axis, originating from the upregulation of PPP2R2C expression to metabolic reprogramming, which ultimately influences the malignant progression and chemotherapy resistance of LUAD. - Source: PubMed
Publication date: 2026/07/16
Chen JiaWang XiaoshanWang ZhengyangLi GangHan Fei - Gestational diabetes mellitus (GDM) is associated with placental dysfunction, which contributes to adverse pregnancy outcomes. This study aimed to compare transcriptomic profiles and immune signatures in placentas from pregnancies with and without GDM. Placental tissues from 22 participants (12 GDM and 10 controls) were analyzed using ribonucleic acid sequencing. Differentially expressed genes were identified and subjected to gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. X-cell analysis was used to assess immune cell composition. Western blotting validated the expression of selected genes. A total of 1045 differentially expressed genes were identified. Among these, COL22A1, COL8A2, ACTC1, PAX6, PPP2R2C, G6PC were significantly upregulated. In contrast, LEP and ERBB2 were downregulated in GDM placentas. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses showed that extracellular matrix organization, muscle contraction, and calcium signaling pathways were upregulated. Pathways involved in glucose import, amino acid transport, and the endoplasmic reticulum (ER) stress response were downregulated. X-cell analysis suggested alterations in stromal and immune cell composition, with increased myocytes and fibroblasts and reduced M2 macrophages in GDM placentas. We found that various molecular signatures, including composition, metabolism, ER stress, and immune cells, were altered in GDM placentas compared to controls. This study demonstrates that the GDM placentas exhibit significant transcriptomic alterations, including changes in metabolic, ER stress-related, and immune pathways. These findings highlight the role of placental remodeling in the pathophysiology of GDM and may provide insights for future research and potential therapeutic strategies. - Source: PubMed
Kang Yea EunLee Seong EunLim Joung YoulKim Ok SoonYoon JiyeonJung YewonLee Ju HeeKu Bon JeongLee MinaKim Hyun Jin - Radiotherapy resistance remains a major obstacle in nasopharyngeal carcinoma (NPC). This study delineates the role of protein phosphatase 2 regulatory subunit B gamma (PPP2R2C) in NPC radioresistance and its underlying mechanism to identify therapeutic targets. Through integrated bioinformatic analysis, PPP2R2C was identified as a candidate radioresistance driver. In vitro and in vivo functional assays demonstrated that PPP2R2C depletion significantly impaired NPC cell proliferation, migration, and radioresistance, while its overexpression enhanced these phenotypes. Mechanistic investigations revealed PPP2R2C inhibits radiation-induced ferroptosis, evidenced by transmission electron microscopy (TEM), lipid reactive oxygen species (ROS) quantification, malondialdehyde (MDA) assays, and immunoblotting of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11). Crucially, immunoprecipitation-mass spectrometry (IP-MS), co-immunoprecipitation (Co-IP), and immunofluorescence (IF) confirmed PPP2R2C physically interacts with RPS27L. Further analysis via qPCR, Western blotting, cycloheximide chase, and proteasome inhibition showed PPP2R2C stabilizes RPS27L protein by blocking proteasomal degradation. RPS27L knockdown reversed PPP2R2C-mediated radioresistance and ferroptosis suppression. Clinically, high PPP2R2C expression correlated with poor patient survival. These findings establish that PPP2R2C promotes NPC radioresistance by stabilizing RPS27L to inhibit ferroptosis, positioning the PPP2R2C-RPS27L axis as a novel prognostic biomarker and therapeutic target for overcoming radioresistance. - Source: PubMed
Publication date: 2026/05/11
Fang JianboYang QiYang LuxiLiu HuiyingHu ShuluShen WeitaoZhang YuemingShen JieWei TingLyu QiongLuo PengWu XiaowenZhang JianMeng Hui - Telomeres and pericentromeres are regions of heterochromatin that are difficult to replicate. Telomeric binding factor 2 (TRF2) is a key telomere protective protein that acts against DNA damage at telomeres and allows the progression of replication forks through telomere chromatin, a region with heterochromatin features that is difficult to replicate. TRF2 is also required at pericentromeres for proper replication elongation. Here, we show that TRF2 positively regulates the activity of protein phosphatase 2A (PP2A) by activating the expression of PPP2R2C, a gene encoding an isoform of the regulatory subunit of PP2A with particularly elevated expression in neuronal tissues. Mechanistically, we provide evidence that TRF2 binds to an intronic interstitial telomeric sequence (ITS) of PPP2R2C with transactivation activity. Moreover, PPP2R2C is recruited to telomeres and pericentromeres during S phase and during replicative stress where it attenuates the DNA damage response. Finally, we show that the TRF2-dependent regulation of PPP2R2C expression plays an important role in maintaining neurodevelopment in zebrafish. These results reveal a mechanism required for normal neurodevelopment by which TRF2 attenuates DNA damage by upregulating PPP2R2C, thereby stimulating PP2A activity at two regions difficult to replicate: telomeres and pericentromeres. - Source: PubMed
Publication date: 2026/01/29
Zhai XiuyunWang CuicuiYing YilinLeong WaiianChen LianxiangWei BohuaCheng XiaojiaoHuang ShengChen QiaowenLu YimingGilson EricYe Jing