PKCγ
- Known as:
- PKCγ
- Catalog number:
- 000323A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PKCγ
Related genes to: PKCγ
- Gene:
- FKBP1A NIH gene
- Name:
- FKBP prolyl isomerase 1A
- Previous symbol:
- FKBP1
- Synonyms:
- FKBP-12, FKBP12, PKC12, PPIASE, FKBP12C
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-14
- Date modifiied:
- 2018-11-01
- Gene:
- HINT1 NIH gene
- Name:
- histidine triad nucleotide binding protein 1
- Previous symbol:
- PRKCNH1, HINT
- Synonyms:
- PKCI-1
- Chromosome:
- 5q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-15
- Date modifiied:
- 2016-10-05
- Gene:
- MARCKS NIH gene
- Name:
- myristoylated alanine rich protein kinase C substrate
- Previous symbol:
- MACS
- Synonyms:
- PKCSL, 80K-L
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1990-01-05
- Date modifiied:
- 2016-06-03
- Gene:
- NME3 NIH gene
- Name:
- NME/NM23 nucleoside diphosphate kinase 3
- Previous symbol:
- -
- Synonyms:
- DR-nm23, NM23-H3, NDPKC
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-19
- Date modifiied:
- 2016-10-05
- Gene:
- PRKCA NIH gene
- Name:
- protein kinase C alpha
- Previous symbol:
- PKCA
- Synonyms:
- PKCα
- Chromosome:
- 17q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-02
- Date modifiied:
- 2018-07-11
Related products to: PKCγ
17 kDa PKC-potentiated inhibitory protein of PP1,Cpi,Cpi17,CPI-17,Ppp1r14a,Protein kinase C-potentiated inhibitor protein of 17 kDa,Protein phosphatase 1 regulatory subunit 14A,Rat,Rattus norvegicus17 kDa PKC-potentiated inhibitory protein of PP1,CPI17,CPI-17,Homo sapiens,Human,PPP1INL,PPP1R14A,Protein kinase C-potentiated inhibitor protein of 17 kDa,Protein phosphatase 1 regulatory subunit 14A17 kDa PKC-potentiated inhibitory protein of PP1,Cpi17,CPI-17,Mouse,Mus musculus,Ppp1r14a,Protein kinase C-potentiated inhibitor protein of 17 kDa,Protein phosphatase 1 regulatory subunit 14A17 kDa PKC-potentiated inhibitory protein of PP1,CPI17,CPI-17,Pig,Protein kinase C-potentiated inhibitor protein of 17 kDa,Protein phosphatase 1 regulatory subunit 14A,Sus scrofaActive PKC ιActive PKC betaIIActive PKC bIIActive PKC bII5 ugActive PKC deltaActive PKC deltaActive PKC deltaActive PKC delta5 ugActive PKC etaActive PKC gammaActive PKC gamma Related articles to: PKCγ
- Cerebral ischemia-reperfusion (I/R) injury is a major cause of stroke-related mortality and disability, primarily driven by mitochondrial dysfunction, oxidative stress, and apoptosis. In this study, we identified phosphorylation of PKCγ at the T655 site following cerebral I/R injury using mass spectrometry. Notably, we observed that approximately 5% of total PKCγ translocates to mitochondria following I/R injury, suggesting a direct role in modulating mitochondrial function. We further investigated the functional role of PKCγ both in vitro and in vivo. Our results demonstrate that the regulatory effects of PKCγ on Nrf2 and mitochondrial function depend on its kinase activity, as evidenced by the lack of effect of the kinase-dead G360S mutant. The phospho-mimetic T655D mutant suppressed Nrf2 nuclear translocation, promoted mitochondrial ROS production, fragmentation, and neuronal apoptosis, whereas the dephospho-mimetic T655A mutant exerted the opposite effects. Nuclear/cytoplasmic fractionation and immunofluorescence analyses further confirmed that PKCγ regulates Nrf2 nuclear translocation in both HeLa cells and primary neurons. Knockdown of PKCγ via shRNA in vitro and AAV9-mediated delivery in mice alleviated mitochondrial dysfunction, reduced infarct volume, and improved neurological outcomes. Behavioral assessments further confirmed the neuroprotective effect of PKCγ knockdown in vivo. Collectively, our findings identify T655 phosphorylation as a key mechanism by which PKCγ regulates mitochondrial dysfunction and oxidative stress during cerebral I/R injury, suggesting that targeting this pathway may represent a promising therapeutic strategy for ischemic stroke. - Source: PubMed
Publication date: 2026/05/27
Li ChenchenChen JinlunOuyang XiangbinDuan RuijiaKuang YijinHe YaohuiTan JieqiongZeng Liuwang - 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