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
- Children with autism spectrum disorder (ASD) often exhibit heightened sensitivity to innocuous mechanical stimuli, such as gentle touch or friction from clothing. However, the neural mechanisms underlying these ASD-associated tactile deficits remain unclear. In the present study, we found that the maternal immune activation (MIA) mouse model of ASD displayed marked mechanical hypersensitivity. Following innocuous mechanical stimulation to the hind paw, protein kinase C gamma (PKCγ) excitatory interneurons were activated in the spinal dorsal horn. Importantly, the activation of PKCγ interneurons contributed to mechanical hypersensitivity in MIA mice. As the density of VGAT (vesicular GABA transporter) inhibitory synapses was significantly reduced in the perisomatic region of PKCγ interneurons, we found obvious activation of spinal microglia and increased microglia-mediated engulfment of inhibitory synapses in the spinal cord of MIA mice. Notably, inhibiting spinal microglia activation not only alleviated mechanical hypersensitivity but also significantly attenuated stereotyped behavior in MIA mice. Together, these results suggest that excessive microglia-mediated phagocytosis of inhibitory synapses increases PKCγ interneuron activation, thereby contributing to mechanical hypersensitivity in MIA mice. Thus, targeting spinal microglia may be a promising therapeutic strategy for alleviating tactile hypersensitivity associated with ASD. - Source: PubMed
Publication date: 2026/05/29
Yao YiweiGu XinyangHuang WenqingHuang ChutianLi BeiZhou JunmeiLi Qian - 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 γ (PKCγ), a Ca2+- and diacylglycerol-dependent Ser/Thr 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 knockin 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 2 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