Ask about this productRelated genes to: Prkch antibody
- Gene:
- PRKCH NIH gene
- Name:
- protein kinase C eta
- Previous symbol:
- PRKCL
- Synonyms:
- PKC-L, PKCL
- Chromosome:
- 14q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-26
- Date modifiied:
- 2016-01-27
Related products to: Prkch antibody
Related articles to: Prkch antibody
- Spinal cord injury (SCI) triggers a complex secondary injury cascade that critically limits neural repair. Although microRNAs have been implicated in post-SCI inflammation and neural regeneration, the key competing endogenous RNA (ceRNA) network regulating immune dysregulation remains unclear. - Source: PubMed
Publication date: 2026/05/07
Yao YuxuanGuo WenliangCai XingyunGui YuchangYao JingzhiLu YutingLiang YuxinWang WenshuTan ZhibiaoZhang JinxiangXu Jianwen - Combination immunotherapies such as atezolizumab plus bevacizumab (Atez/Bev) and durvalumab plus tremelimumab (Dur/Tre) improve outcomes in advanced hepatocellular carcinoma (HCC), yet systemic immune mechanisms underlying response remain incompletely defined. - Source: PubMed
Publication date: 2026/03/30
Nishio AkiraKodama TakahiroDaiku KazumaMaesaka KazukiTanaka SatoshiNozaki YasutoshiKurahashi TomohideMatsumoto KengoNawa TakatoshiTawara SeiichiTokuda YukiNakabori TasukuSakamori RyotaroOhkawa KazuyoshiMiyazaki MasanoriYamamoto ShuheiShigeno SatoshiMyojin YutaTahata YukiHikita HayatoTakehara Tetsuo - CEU-938, an innovative antimicrotubule prodrug bioactivated by cytochrome P450 1A1 (CYP1A1), represents a promising targeted alternative for cancer cells overexpressing this enzyme. To optimize its clinical utility and minimize off-target effects in breast cancer (BC) patients, this study aims to identify predictive biomarkers of CEU-938 efficacy. The antiproliferative activity of CEU-938 was assessed across a panel of 39 human breast cancer and non-tumorigenic cell lines. Differential expression analyses were subsequently performed to distinguish CEU-938-responsive from non-responsive cell lines using a threshold of 1000 nM. Candidate biomarkers identified through this approach were then validated by RT-qPCR and Western blot analyses. CEU-938 demonstrated marked and selective antiproliferative activity across molecular subtypes of human breast cancer, with efficacy observed in approximately 40% of triple-negative breast cancer (TNBC), 70% of estrogen receptor-positive (ER), and 80% of human epidermal growth factor receptor 2-positive (HER2) breast cancer cell lines, while sparing non-tumorigenic human breast cells (MCF 10A, MCF-12A, 184B5). Differential expression analysis identified five candidate biomarkers associated with CEU-938 responsiveness, namely, FOXA1 (log2-fold change (LFC) = 3.1), RAB25 (LFC = 3.8), RHOV (LFC = 2.9), PRKCH (LFC = 1.6), and HDAC9 (LFC = -1.7). Among these, FOXA1 and RAB25 robustly validated by RT-qPCR and Western blot analyses, showing strong inverse correlations with CEU-938 sensitivity (Spearman correlation coefficients of -0.82 and -0.61, respectively, at the protein level). The predictive value of FOXA1 and RAB25 was further confirmed by Western blot analyses in two independent breast cell line models, the non-responsive MCF-12A and the responsive MDA-kb2. Collectively, these findings identify FOXA1 and RAB25 as robust predictive biomarkers of response to CEU-938. Notably, FOXA1 and RAB25 are strongly implicated in breast cancer biology, and FOXA1 has been directly linked to the aryl hydrocarbon receptor (AHR), the main regulator of CYP1A1. These results position CEU-938 as a strong precision-therapy candidate that combines target selectivity, a favorable toxicity profile, and biomarker-enabled patient stratification, with potential clinical benefit in ER and HER2 enriched tumors, as well as a subset of TNBC. - Source: PubMed
Publication date: 2026/02/25
Bruxelles QuentinHamel-Côté GenevièveScott-Boyer Marie-PierOuellette VincentC-Gaudreault RenéDurocher FrancineDiorio CarolineDroit ArnaudFortin Sébastien - Amelogenin, essential for enamel formation, is encoded by the alternatively spliced gene Amelx/AMELX, with exon4 splicing producing major protein isoforms and a microRNA (miR-exon4). We previously reported that miR-exon4 regulates osteoblast and ameloblast function via the Nfia- and Prkch-Runx2 axis and may be involved in X-linked Amelogenesis Imperfecta associated with exon4 splicing defects. This study investigates miR-exon4’s role in enamel defect development and exon4 splicing. A miR-exon4 mimic or inhibitor was applied to mouse pups during enamel development. One-week inhibition of miR-exon4 reduced enamel mineralization, shortened the early mineralization phase, and lowered RUNX2 expression, leading to increased Amelx mRNA and amelogenin protein levels. A 24-hour inhibition enhanced exon4 splicing without affecting overall Amelx expression, suggesting a direct role in splicing regulation. MiR-exon4 inhibition also altered the expression of Serine/Arginine-rich splicing factors (SRSFs), indicating indirect modulation of exon4 splicing. Nuclear localization of miR-exon4 was confirmed using an Amelx minigene, and a mutant form that reduced nuclear miR-exon4 levels impaired its binding to Amelx pre-mRNA. A binding site of miR-exon4 at the intron4 branch point further supports its direct involvement in exon4 splicing. These findings suggest a role for miR-exon4 in regulating both amelogenin expression and exon4 splicing, leading to enamel defects when absent. - Source: PubMed
Publication date: 2026/02/25
Shemirani RozanaDuong TrangKim RebeccaShetty AnkithaAnsel K MarkNakano Yukiko - Triple-negative breast cancer (TNBC) is an aggressive disease characterized by high metastatic potential and limited treatment options. Protein kinase C-eta (PKCη), an antiapoptotic kinase of the novel PKC subfamily, is associated with poor prognosis in breast cancer patients. Analysis of TNBC tumors revealed that PRKCH (PKCη) expression is linked to an epithelial‒mesenchymal transition (EMT) signature, which is indicative of a metastatic phenotype. Using genetic ablation studies, we showed that PKCη promotes metastasis by enhancing EMT and stemness. Notably, compared with those in PKCη-intact tumors, orthotopic xenografts of PKCη-knockout cells in NSG mice resulted in reduced tumor growth and metastasis. Mechanistically, PKCη functions as a negative regulator of the Hippo pathway by activating YAP. PKCη phosphorylates YAP at Ser128, leading to its stabilization and nuclear translocation, which promotes metastasis. We also demonstrated that PKCη negatively regulates AKT, thereby further sustaining the downregulation of the Hippo pathway. Finally, we show that an evolutionarily conserved peptide encoded by an upstream open reading frame (uORF) preceding the PKCη coding sequence functions as a PKCη degrader, activating the Hippo pathway and promoting YAP degradation. Together, our findings reveal a PKCη-driven signaling axis that regulates the Hippo-YAP pathway in TNBC metastasis, highlighting the potential therapeutic vulnerability of this aggressive disease. - Source: PubMed
Publication date: 2026/02/17
Liju Vijayasteltar BWaidha KamranMuraleedharan AmithaJayaram Divya RamHaimov HodayaJagadeeshan SankarManikandan Dinesh BabuShareb Raghda AbuNurukurti LivingstoneSklarz MenachemGutkind J SilvioAllon IritCohen OfirElkabets MosheLivneh Etta