Ask about this productRelated genes to: PRKCE antibody
- Gene:
- PRKCE NIH gene
- Name:
- protein kinase C epsilon
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2016-01-27
Related products to: PRKCE antibody
Related articles to: PRKCE antibody
- The mechanism by which cigarette smoking affects bladder cancer susceptibility via glucose metabolism remains unclear. We identified bladder cancer-specific glucose metabolism-related genes (GMGs) using Molecular Signatures Database (MSigDB) and a case-control study (580 cases and 1,101 controls) through genetic association and interaction analyses with cigarette smoking. Among 811 GMGs, we observed that rs4953292 G > A was significantly associated with increased bladder cancer risk [odds ratio (OR) = 1.19, 95% confidence interval (CI): 1.03-1.37, = 1.87 × 10] and exhibited an interaction effect with cigarette smoking ( < 0.05). Smokers with rs4953292 A allele had higher bladder cancer risk than nonsmokers with G allele ( < 9.09 × 10). We performed functional experiments using 4-aminobiphenyl (4-ABP)-treated bladder cancer cells and found that the rs4953292 A allele combined with 4-ABP decreased expression levels in bladder cancer cells, which could upregulate PKG and phosphorylate VASP within the cGMP-PKG signaling pathway, enhance glucose uptake, lactate generation, and extracellular acidification rate (ECAR) to reprogram glycolysis, thus promoting bladder cancer susceptibility. This study elucidates that cigarette smoking-regulated facilitates bladder cancer susceptibility by mediating glycolytic reprogramming through activating the cGMP-PKG signaling pathway. The findings provide valuable predictors for bladder cancer susceptibility, aiding in prevention strategies. - Source: PubMed
Publication date: 2025/12/29
Xiao YanpingZhang JinyueJia YuSong HuiMao ZhenguangGao FangZheng Rui - Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related death, and patients usually exhibit impaired immune function within the tumor environment. NSD2 is an H3K36 methyltransferase and has been considered a cancer-promoting factor. However, the role of NSD2 in the occurrence and development of HCC is still unclear. In this study, the effects of NSD2 on HCC were assessed by both mouse and cell models. RNA-seq, ChIP-seq, and orthotopic tumor models were employed to decipher the downstream mechanisms of NSD2 responsible for HCC development. NSD2 alterations were characterized in patients with HCC. Hepatocyte-specific NSD2 overexpression suppresses the proliferation of tumor cells in DEN-treated mice. Mechanistically, NSD2 inhibits OXPHOS by activating target genes (Camk2d and Prkce) transcription. Downregulation of OXPHOS, caused by overexpression of NSD2, inhibits the expression of PD-L1 and enhances immune recognition of tumors. What's more, inhibition of OXPHOS suppresses the formation of HCC. Finally, patients with low expression of NSD2 have a better response to PD-L1 inhibitor treatment. These findings showed that NSD2 inhibits the progression of HCC by inhibiting the expression of PD-L1 through OXPHOS. Our results identify NSD2 as a tumor suppressor in the development of HCC. - Source: PubMed
Publication date: 2026/02/27
Zhang WeiFeng WenxinMa ChunxiaoRao HanyuLiu ChangweiXu YueLiu NingyuanWang ZiyiAji RebiguliHan TingGao Wei-QiangXiao XiuyingLi Li - Chronic joint pain in rheumatoid arthritis (RA) represents a persistent therapeutic challenge, and although luteolin (LUT) exhibits established anti-inflammatory properties, its precise mechanism for alleviating RA-associated chronic pain remains undefined. Through systematic investigation in collagen-induced arthritis (CIA) mice, we demonstrated that LUT administration effectively attenuated chronic pain by modulating spinal cluster of differentiation 4 positive T (CD4 T) cell dynamics and suppressing microglial activation. Integrated multi-omics profiling (cleavage under targets and tagmentation (CUT&Tag), RNA sequencing (RNA-seq), and metabolomics) coupled with functional validation revealed nuclear factor of activated T cells 2 (NFATC2) as the central transcriptional regulator governing T helper 17 (Th17) cell differentiation and spinal infiltration through protein kinase C epsilon (PRKCE)-signal transducer and activator of transcription 3 (STAT3) signaling transduction. Significantly, our mechanistic studies uncovered a previously unrecognized epigenetic cascade: LUT-mediated suppression of lactate dehydrogenase A (LDHA) activity disrupts glycolysis-fueled histone 3 lysine 9 lactylation (H3K9la), thereby epigenetically silencing NFATC2 transcription. Translational studies using RA patient-derived CD4 T cells confirmed LUT's capacity to normalize pathological hyperactivity of the LDHA/H3K9la/NFATC2 axis, concomitantly regulating CD4 T dynamics. Biophysical validation through molecular docking, surface plasmon resonance (SPR), and molecular dynamics (MD) simulations established LUT's direct binding to LDHA with high affinity. Collectively, these findings delineate a novel therapeutic paradigm wherein LUT alleviates RA-associated chronic pain by orchestrating Th17 differentiation and migratory capacity through coordinated blockade of the LDHA-H3K9la-NFATC2 signaling network, highlighting its potential as a disease-modifying agent for chronic pain management in RA. - Source: PubMed
Publication date: 2025/06/20
Jiang YuepengZhao YangMa XiaoZhao XiaoxuanZheng MengjiaWen JunjunYuan CunruiDing XinyiWen Chengping - This study aimed to investigate the impact of the RNA-binding protein eukaryotic translation initiation factor 2-alpha kinase 2 (EIF2AK2) gene, also known as PKR, on the condition of islet beta cells. In this study, EIF2AK2 was overexpressed in INS1 cells, and transcriptome data following EIF2AK2 overexpression were obtained using RNA-seq technology. Additionally, potential target genes that bind to EIF2AK2 were identified through iRIP-seq technology. The proteins interacting with EIF2AK2 were characterized using co-immunoprecipitation (CO-IP) combined with mass spectrometry to elucidate the molecular regulatory mechanisms of EIF2AK2 in INS1 cells. RNA-seq results indicated that in INS1 cells overexpressing EIF2AK2, 1171 genes were differentially expressed, and 2161 alternative splicing events were significantly altered. iRIP-seq data demonstrated that reads from the immunoprecipitated samples were significantly enriched in the intronic and coding sequence (CDS) regions. EIF2AK2 preferentially binds to the GCGGCGG motif in RNA. Comprehensive analysis suggests that EIF2AK2 may directly bind to and regulate the expression of Dusp8, Btg1, and Prkce, thereby affecting pancreatic islet cell functions. Furthermore, EIF2AK2 may influence islet cell function by modulating the alternative splicing of Zfr and Pias2. Additionally, combined with Co-IP mass spectrometry data, it was discovered that EIF2AK2 can interact with 649 proteins, including various differentially expressed RNA-binding proteins, transcription factors, and histones, which may be associated with diabetes. Our results indicate that EIF2AK2 may regulate the expression or alternative splicing of mRNA related to type 2 diabetes through direct or indirect binding. Additionally, it may influence the progression of type 2 diabetes by interacting with other proteins. We propose that EIF2AK2 plays a significant role in diabetic islet beta cells, and its aberrant regulatory pattern is closely associated with the onset and progression of type 2 diabetes. - Source: PubMed
Ning LiliLiu TongLv YuanyuanCheng YanYang MaoguangCai Hanqing - Clear cell renal cell carcinoma (ccRCC) is a prevalent urological malignancy, accounting for approximately 1.6% of all cancer-related deaths in 2022. While endocrine-disrupting chemicals (EDCs) have been implicated as risk factors for ccRCC, the toxicological profiles and immune mechanisms underlying Bisphenol A (BPA) exposure in ccRCC progression remain inadequately understood. Protein-protein interaction (PPI) analysis and visualization were performed on overlapping genes between ccRCC and BPA exposure. This was followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to elucidate potential underlying mechanisms. Subsequently, 108 distinct machine learning algorithm combinations were evaluated to identify the optimal predictive model. An integrated CoxBoost and Ridge regression model was constructed to develop a prognostic signature, the performance of which was rigorously validated across two independent external datasets. Finally, molecular docking analyses were employed to investigate interactions between key genes and BPA. A total of 114 overlapping targets associated with both ccRCC and BPA were identified. GO and KEGG analyses revealed enrichment in cancer-related pathways, including pathways in cancer, endocrine resistance, PD-L1 expression and PD-1 checkpoint signaling, T-cell receptor signaling, endocrine function, and immune responses. Machine learning algorithm selection identified the combined CoxBoost-Ridge approach as the optimal predictive model (achieving a training set concordance index (C-index) of 0.77). This model identified eight key genes (, , , , , , , ), which were the top-ranked by coefficient magnitude in the prognostic model. The prognostic signature demonstrated robust predictive performance in two independent external validation cohorts (C-index = 0.74 in cBioPortal; C-index = 0.81 in E-MTAB-1980). Furthermore, molecular docking analyses predicted strong binding affinities between BPA and these key targets (Vina scores all <-6.5 kcal/mol), suggesting a potential mechanism through which BPA may modulate their activity to promote renal carcinogenesis. Collectively, These findings suggested potential molecular mechanisms that may underpin BPA-induced ccRCC progression, generating hypotheses for future experimental validation. These findings enhance our understanding of the molecular mechanisms by which BPA induces ccRCC and highlight potential targets for therapeutic intervention, particularly in endocrine and immune-related pathways. This underscores the need for collaborative efforts to mitigate the impact of environmental toxins like BPA on public health. - Source: PubMed
Publication date: 2025/11/13
Chen JieRan BiaoChen BoBai JingxingJian ShiboHuang YinYang JiahaoLi JinzeChen ZeyuWei QiangAi JianzhongLiu LiangrenCao Dehong