Ask about this productRelated genes to: PRKCG antibody
- Gene:
- PRKCG NIH gene
- Name:
- protein kinase C gamma
- Previous symbol:
- PKCG, SCA14
- Synonyms:
- PKCC, MGC57564, PKCγ
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-02
- Date modifiied:
- 2019-04-23
Related products to: PRKCG antibody
Related articles to: PRKCG antibody
- The application of molecular techniques has significantly refined the classification of cutaneous mesenchymal tumors, uncovering recurrent genetic alterations that aid in diagnostically challenging cases. Dermatofibroma, or cutaneous fibrous histiocytoma, is a common benign neoplasm with broad morphologic variability and limited immunohistochemical specificity, for which recurrent protein kinase C gene fusions have recently been described. We report a novel case of a cellular, pseudoangiomatous DF arising on the dorsum of a 56-year-old man and harboring an in-frame MYADM::PRKCG fusion transcript. Histologically, the lesion displayed high cellularity and prominent vascularity, and focal smooth muscle actin and desmin positivity, initially suggesting angiomatoid fibrous histiocytoma. Targeted RNA sequencing identified a previously unreported MYADM::PRKCG fusion, enabling definitive classification. This is the first description of a MYADM::PRKCG rearrangement in DF, further expanding our knowledge about the molecular landscape of this neoplasm. - Source: PubMed
Publication date: 2026/05/06
Della Mura MarioKrimchansky OrenRizzo AlessandroTrilli IrmaSalzillo CeciliaFortarezza FrancescoPaolo Dei Tos AngeloYang Richard KCheal Cho WooCazzato Gerardo - Pancreatic adenocarcinoma (PAAD) is a highly lethal malignancy with limited prognostic biomarkers and therapeutic targets. Lactate-driven lactylation has recently emerged as an important regulator of cancer progression, but its role in PAAD remains unclear. In this study, integrative analysis of TCGA and GEO datasets, combined with experimental validation, identified a five-gene lactylation-associated signature (LRP3, TTLL6, TSGA13, PRKCG, and SDK2) that effectively stratified PAAD patients by survival risk. High-risk tumors displayed an immunosuppressive phenotype with reduced immune infiltration, Th2-skewed remodeling, checkpoint activation, and distinct mutational and drug-sensitivity features. Among the signature genes, PRKCG was significantly downregulated in PAAD and associated with advanced disease and worse prognosis. PRKCG overexpression inhibited tumor cell proliferation, migration, invasion, and xenograft growth, while enhancing apoptosis. Mechanistically, lactate-induced lactylation impaired PRKCG-dependent activation of the p53 pathway without altering PRKCG expression, and mutation of predicted lactylation sites partially rescued this effect. These findings define a lactylation-associated prognostic model for PAAD and highlight the lactate-PRKCG-p53 axis as a potential therapeutic vulnerability. - Source: PubMed
Publication date: 2026/04/24
Zhu WenboMa CongjiaZhao XintongSong YingxiaoLi JiayiFeng YongpuSun FengyuanLi ZhaoshenDu YiqiKong XiangyuKong Fanyang - Ulcerative colitis (UC) is a significant and challenging condition in the digestive system, necessitating the development of effective therapeutic interventions. The Daifu decoction (DFD) is derived from the Lizhong decoction, a classic traditional Chinese Medicine (TCM) formula used to treat digestive diseases. Previous studies have found that DFD has a clear therapeutic effect on UC. This study aimed to investigate the underlying mechanisms of DFD in UC treatment. - Source: PubMed
Publication date: 2026/03/24
Zhao YangyangCui DanyangGong YangXiao Yanan - Spinocerebellar Ataxia Type 14 (SCA14) is an autosomal dominant neurodegenerative disease caused by mutations in the gene encoding protein kinase C gamma (PKCγ), a Ca2+/diacylglycerol (DG)-dependent serine/threonine kinase dominantly expressed in cerebellar Purkinje cells. These mutations impair autoinhibitory constraints to increase the basal activity of the kinase, resulting in deficits in the cerebellum that are not observed upon simple deletion of the gene, and severe ataxia. To better understand the impact of aberrant PKCγ signaling in disease pathology, we developed a knock-in murine model of the SCA14 mutation ΔF48 in PKCγ. This fully-penetrant mutation is severe in humans and is mechanistically informative as it has high basal activity but is unresponsive to agonist stimulation. Genetic, behavioral, and molecular testing revealed that ΔF48 PKCγ mice have ataxia-related phenotypes and an altered cerebellar phosphoproteome driven primarily by enhanced Ca2+/calmodulin-dependent Kinase II (CaMKII) signaling, effects that were more severe in male mice. Analysis of existing human data revealed that SCA14 has a significantly earlier age of onset for males compared with females. Data from this clinically relevant mutation suggested that enhanced basal activity of PKCγ is sufficient to cause ataxia and that treatment strategies to modulate aberrant PKCγ may be particularly beneficial in males. - Source: PubMed
Publication date: 2026/04/02
Wolfe Sarah AMa YuliangYaron-Barir Tomer MChang CarlyPilo Caila AGhassemian MajidRoberts Amanda JLee Sang RyeulHenson Benjamin AJepsen KristenJohnson Jared LCantley Lewis CTaylor Susan SGorrie GeorgeNewton Alexandra C - Prolonged occupational exposure to oil mist particulate matter (OMPM) poses health risks, yet its neurotoxic effects and underlying mechanisms remain poorly understood. Here, OMPM generated from turbine oil commonly used in occupational labor environments was used to expose rats. The rats were divided into the control and OMPM groups. Following 42 days of exposure, a multidimensional assessment was performed using untargeted metabolomics, phosphoproteomics, behavioral testing, hematoxylin-eosin (HE) staining, transmission electron microscopy (TEM), colorimetric assays, enzyme-linked immunosorbent assay, and Western blotting (WB) to evaluate metabolic alterations, protein phosphorylation, and tissue integrity in the striatum. Integrated omics analyses revealed that differentially phosphorylated proteins and metabolites were remarkably enriched in dopaminergic synapse, Parkinson's disease, and amphetamine addiction pathways (FDR < 0.05), with a regulatory axis involving L-tyrosine, tyrosine hydroxylase (TH), and dopamine (DA) identified. OMPM-exposed rats exhibited depression- and anxiety-like behaviors, alongside striatal pathological and ultrastructural damage. Biochemical analyses showed elevated malondialdehyde and reactive oxygen species levels; reduced superoxide dismutase, glutathione, and glutathione peroxidase activities and total antioxidant capacity; increased glutathione disulfide and inducible nitric oxide synthase expression; and decreased DA and L-tyrosine levels. Additionally, proinflammatory mediators (IL-1β, IL-6, TNF-α, MCP-1, and PGD) were significantly upregulated in the striatum. WB analysis further confirmed significant reductions in the relative phosphorylation levels of key regulators in dopaminergic and calcium signaling pathways, including CALM3, CaMK2b, GSK-3β, PRKCG, and TH. Collectively, these findings reveal critical molecular and biochemical alterations in the rat striatum following OMPM exposure and provide a mechanistic basis for understanding depression-like behaviors associated with prolonged OMPM exposure in occupational workers. - Source: PubMed
Publication date: 2026/03/12
Nie HuipengLiu XuanShi YueLiu HuanliangLai WenqingLi KangTian LeiXi ZhugeLin Bencheng