Ask about this productRelated genes to: PRKCZ antibody
- Gene:
- PRKCZ NIH gene
- Name:
- protein kinase C zeta
- Previous symbol:
- -
- Synonyms:
- PKC2
- Chromosome:
- 1p36.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2016-10-05
Related products to: PRKCZ antibody
Related articles to: PRKCZ antibody
- Osteoporosis is characterized by disrupted bone homeostasis while dysregulated autophagy contributes to impaired bone remodeling and bone loss. This study investigates the role of the RNA-binding protein polypyrimidine tract binding protein 1 (PTBP1) in osteoporosis progression through regulation of protein kinase C zeta (PRKCZ), and elucidates whether PTBP1 modulates the osteogenic-adipogenic fate commitment of bone marrow mesenchymal stem cells (BMSCs) via autophagy. - Source: PubMed
Publication date: 2026/08/12
Wang ChenSun JianDong Meng - Hypospadias is one of the most common birth defects in China and a key feature of differences in sex development (DSD), yet its genetic etiology remains largely unresolved. Current diagnostic approaches using DSD-targeted gene panels have a low rate of definitive diagnoses (5.5%), highlighting the need for more comprehensive genetic investigation. In this study, we performed next-generation sequencing (NGS) on the largest trio-based cohort of hypospadias to date, comprising 106 pediatric cases and their parents (92 trios). We achieved a definitive genetic diagnosis in 6.6% of patients, identifying pathogenic variants in canonical DSD genes such as AR, NR5A1 and WT1. By incorporating a broader spectrum of potentially clinically significant variants, we increased the overall genetic identification rate to 33.0% (35/106). Strikingly, trio analysis uncovered a significant burden of de novo loss-of-function (LoF) variants (2.2-fold enrichment, P=0.001), primarily driven by variants in genes associated with ciliopathies (10.35-fold, P=0.016), a previously underappreciated gene class in hypospadias. Furthermore, we identified and functionally validated two high-confidence risk genes, PRKCZ and HRNR, based on recurrent de novo variants. Functional assays confirmed that these variants disrupt key biological mechanisms, including cell proliferation, migration, and androgen signaling. Our large-scale trio approach substantially expands the genetic landscape of hypospadias, demonstrates the critical value of trio-based sequencing for improving diagnostic yield, and decisively implicates ciliary genes in its pathogenesis. - Source: PubMed
Publication date: 2026/07/23
You YanqinLuo YingliuZhou HonghuiLiang QiaoweiXue JingjieLi ZhuoZhao YaowangHe TianquWang KexinWang HongyanChen ZhongzhongWu Lingqian - Fibro-adipogenic progenitor (FAP) dysfunction drives skeletal muscle fibrosis in type 2 diabetes mellitus (T2DM), yet the underlying metabolic-epigenetic mechanisms remain poorly understood. This study investigates how metabolite fluctuations regulate the cell fate of CD90 FAPs in the diabetic skeletal muscles. - Source: PubMed
Publication date: 2026/08/10
Tong Zhou-JieLi Yi-HuiSong MingSheng Ya-NanWu Yan-ZhaoShang Yuan-YuanHu Bo-AngLu BinZhu PingWang Gan-QiZhan Hao-JieHan LuZhang WeiWang Zhi-HaoZhong Ming - IntroductionDysregulation of apoptosis is a hallmark of follicular lymphoma (FL), yet the causal genetic drivers remain incompletely understood. This study aimed to identify causal apoptosis-related genes in FL and validate their functional roles.MethodsWe conducted a multi-omics Mendelian randomization (MR) study, integrating summary statistics from a large-scale FL genome-wide association study with data on methylation (mQTL), expression (eQTL), and protein (pQTL) quantitative trait loci. Summary data-based MR (SMR) and colocalization analyses were used to identify candidate causal genes. Independent external transcriptomic cohorts were utilized to validate the gene correlations, and evaluate the clinical prognostic relevance of the identified candidates. Key findings were then validated in FL patient tissues using RT-qPCR, and the functional role and downstream molecular mechanisms of the top candidate gene were systematically characterized through phenotypic characterization, drug sensitivity testing, and mechanistic signaling analyses.ResultsOur MR analysis identified several genes with causal links to FL risk, with integrative analysis highlighting , , and Notably, and exhibited significant correlation, whereas displayed an independent regulatory pattern. Clinical tissue validation confirmed that mRNA levels were significantly elevated in FL patient tissues. Functional studies in an FL cell line demonstrated that acts as an oncogene, promoting proliferation, colony formation, and migration while inhibiting apoptosis. Mechanistically, depletion promoted FOXO1-mediated transcriptional upregulation of CD20 via the XBP1/FOXO1 signaling axis, which concomitantly activated the intrinsic apoptotic pathway and significantly enhanced the sensitivity of FL cells to Rituximab-mediated cytotoxicity and apoptosis.Additionally, survival analysis revealed that serves as a strong prognostic indicator, with its low expression correlated with poorer progression-free survival and overall survival in FL patients.ConclusionsThis study provides the genetic and functional evidence establishing as a novel causal oncogene in the pathogenesis of FL. Our findings elucidate the critical role of the IER3IP1-mediated XBP1/FOXO1/CD20 axis in targeted therapy resistance, highlighting as a promising therapeutic target to restore apoptotic activity and improve Rituximab sensitivity. - Source: PubMed
Publication date: 2026/07/23
Zhu BinWang SuliZhao Wenli - Bladder cancer (BCa) is a highly prevalent urological malignancy and one of the most frequently occurring cancers worldwide, necessitating the development of diagnostic and therapeutic biomarkers. This study aimed to explore candidate genes that may be involved in the carcinogenesis of BCa. - Source: PubMed
Publication date: 2026/07/18
Sajjadi SanaRamezani AminAlavimanesh SajadAlipoor HojatTakhshid Mohammad Ali