Ask about this productRelated genes to: PPP1R14B antibody
- Gene:
- PPP1R14B NIH gene
- Name:
- protein phosphatase 1 regulatory inhibitor subunit 14B
- Previous symbol:
- PLCB3N
- Synonyms:
- SOM172, PNG, PHI-1
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-29
- Date modifiied:
- 2016-10-05
Related products to: PPP1R14B antibody
Related articles to: PPP1R14B antibody
- Resistance to immune checkpoint inhibitors (ICIs) in prostate cancer (PCa) is driven by a "cold" tumor immune microenvironment. Astragaloside IV (AS-IV), a major bioactive saponin isolated from Astragalus membranaceus, exhibits immunomodulatory potential, yet its direct molecular targets remain elusive. Concurrently, PPP1R14B is overexpressed in PCa, but its role in mediating immune evasion is unclear. - Source: PubMed
Publication date: 2026/04/04
Yang JieWang JiaZhang WenboHe HanWang ChaoZhang YunfengZhou Fenghai - The diamondback moth (DBM) is a major global pest of cruciferous crops. Silk production, essential for DBM larval locomotion and pupal attachment, is governed by fibroin heavy chain (FibH), fibroin light chain (FibL), and fibrohexamerin (P25). However, the regulatory mechanisms and downstream key genes involved in silk production in DBM remain poorly understood. To address this, we integrated transcriptomic and proteomic data from CRISPR/Cas9 generated PxFibH, PxFibL, and PxP25 mutants to investigate the impact of silk gene deletions in the silk gland and identify modulators of silk formation. In the transcriptomic analysis, we identified 1994, 913, and 1266 differentially expressed genes (DEGs) in the three mutant strains, respectively. GO and KEGG enrichment analysis revealed significant involvement in pathways such as oxidation-reduction process, transmembrane transport, enzyme activity, and extracellular matrix (ECM) receptor interaction. At the proteomic level, 604, 210, and 266 differentially expressed proteins (DEPs) were identified in the three mutants, respectively. GO and KEGG enrichment analysis of these DEPs consistently highlighted energy metabolism, hydrolase activity, and catalytic activity pathways. Integrated multi-omics analyses identified three conserved regulator genes: cytochrome c oxidase subunit 6A1 (COX6A1), N-acetylneuraminate lyase (NAL), and protein phosphatase 1 regulatory subunit 14B (PPP1R14B). CRISPR/Cas9 knockout of PxCOX6A1 resulted in incomplete cocoon formation, along with increased larval mortality, prolonged development, and reduced oviposition. PxNAL knockout was lethal, while heterozygotes exhibited decreased cocoon formation, pupal weight, and fecundity. This study reveals FibH/FibL/P25-dependent metabolic networks regulating silk production and identifies COX6A1 and NAL as novel targets for environmentally sustainable pest control strategies. - Source: PubMed
Publication date: 2025/10/17
Niu Rui-ChangZeng Qing-HuiWang Wen-JingHu JiaLiu Tong-XianZhang Shi-Ze - Disulfidptosis, a new identified form of regulated cell death, has been implicated in cancer. However, the mechanisms through which disulfidptosis-related long noncoding RNAs (lncRNAs) predict prognosis in cervical cancer (CC) remain unclear. Here, we identified disulfidptosis-related genes and lncRNAs in the cancer genome atlas database. Least absolute shrinkage and selection operator and Cox regression analyses were used to construct a prognostic risk signature based on optimal disulfidptosis-related lncRNAs. The prognostic performance of the signature was evaluated using Kaplan-Meier survival analysis and receiver operating characteristic curves. Correlation between the risk signature, gene mutation landscape, tumor immune microenvironment, and immunotherapy or chemotherapy sensitivity was determined. Additionally, the expression levels of disulfidptosis-related lncRNAs in CC were validated by quantitative PCR. A total of 403 disulfidptosis-related lncRNAs were identified, among which 9 disulfidptosis-related lncRNAs were used to construct a prognostic risk signature that classified patients with CC into high-risk and low-risk groups. Kaplan-Meier, receiver operating characteristic curves, and the concordance index demonstrated that the risk signature exhibited good sensitivity and specificity. The low-risk group exhibited improved survival outcomes and increased sensitivity to immunotherapy, whereas the high-risk group showed heightened sensitivity to to bexarotene, bicalutamide, embelin, FH535, and pazopanib. Quantitative PCR results indicated that ILF3-DT and PPP1R14B-AS1 were downregulated in CC tissues, whereas RUSC1-AS1 was upregulated. In conclusion, we developed a novel prognostic risk signature based on 9 disulfidptosis-related lncRNAs, which may serve as an independent predictor of immunotherapy response and chemotherapy sensitivity in CC. - Source: PubMed
Zhao HuGuo YilinWang LuLi RuiWang Yingmei - All-trans retinoic acid (atRA), a potent derivative of vitamin A, is recognized as a significant teratogen for inducing cleft palate in both humans and mice. The molecular mechanisms underlying it remain intricate and incompletely elucidated. The advent of single-cell sequencing technology offers novel methodologies to investigate the mechanisms by which atRA induces cleft palate. In this study, we use C57BL/6 mice to conduct cleft palate models, comprising a control group and an atRA-exposed group. Palatal shelves were collected at embryonic day 12.5 (E12.5) for 10x single-cell sequencing analysis to discern and compare the cellular and molecular disparities between the two groups. Validation of the findings was performed using Quantitative real-time polymerase chain reaction and Western blot techniques. The findings indicate that at E12.5, atRA predominantly affects the mesenchymal and epithelial cells of the palatal shelves, inhibiting cellular proliferation and migration. The primary mechanism of atRA's effect involves modulation of the Wnt and TGF-β signaling pathways. Furthermore, the Ppp1r14b gene was identified as a critical mediator in atRA's interaction with these pathways. This study provides a more comprehensive understanding of the mechanisms underlying atRA-induced cleft palate formation. It highlights the significance of the Wnt and TGF-β pathways, as well as the Ppp1r14b gene during this procedure. - Source: PubMed
Publication date: 2025/11/20
Ma YapingWang BinqingGao ShikangSong Tao - Prostate cancer (PCa) is the tumor with the highest incidence rate among men worldwide. There is still a lack of effective treatment options for metastatic PCa and castration-resistant prostate cancer (CRPC). Protein phosphatase 1 regulatory subunit 14B (PPP1R14B) has been found to be associated with the occurrence and development of various cancers. However, the role and mechanism of PPP1R14B in PCa have not yet been deeply explored. Here, we found that PPP1R14B was highly expressed in PCa tissues and was significantly associated with a higher Gleason score and clinical T stage. Knockdown of PPP1R14B significantly inhibited the proliferation, migration and invasion abilities of PCa cells, while overexpression of PPP1R14B produced the opposite effect. Mechanistic investigations revealed that PPP1R14B mainly regulates the expression of AR through the JAK2/STAT3 pathway and forms a positive feedback loop with STAT3 to promote the progression of PCa, reduce the sensitivity of tumors to enzalutamide, and accelerate the formation of drug resistance. In addition, genistein, a drug screened through virtual drug prediction and molecular alignment, mainly inhibits the expression of STAT3 by targeting PPP1R14B. Moreover, when combined with STAT3-IN-13, it can more effectively curb the malignant ability of PCa and enhance the sensitivity of tumor cells to enzalutamide. In conclusion, these findings reveal the function and mechanism of PPP1R14B in the progression of PCa and the resistance of enzalutamide, indicating that PPP1R14B is a potential target for the treatment of PCa and the prospect of genistein as a therapeutic drug. - Source: PubMed
Publication date: 2025/10/09
Cheng LongYou ChengyuMa LongtuLiu ShuaiLao YongfengGuan XinWang WenyunXiao XiTao YanDong Zhilong