Ask about this productRelated genes to: PRKCG Blocking Peptide
- 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 Blocking Peptide
Related articles to: PRKCG Blocking Peptide
- The cerebellum relies on Purkinje cells (PCs) to coordinate motor functions and maintain neural circuitry. Impaired PC dendritogenesis is linked to neurological disorders, yet intrinsic molecular mechanisms remain unclear. We demonstrate that postnatal deletion of Yin Yang 1 () in PCs disrupts dendrite and spine formation, impairs synaptic plasticity, and alters protein kinase C gamma (PKCγ) expression, leading to cerebellar ataxia and progressive atrophy. Mechanistically, YY1 transcriptionally activates wingless-type MMTV integration site family, member 10B (), which signals through Frizzled-4 (Fzd4) in PCs. downregulation mimics the dendritic defects seen in mutants, indicating its crucial role in dendrite growth and synaptic environment regulation. These changes result in defective synapse innervation. Our findings reveal that YY1 governs PC dendritogenesis and synaptogenesis via , while also modulating PKCγ and β-catenin signaling. The YY1-Wnt10b axis emerges as a critical pathway underlying YY1-associated cerebellar dysfunction. - Source: PubMed
Publication date: 2026/07/31
Lui Ying LamDong XiaonanLeung Thomas Chun NingLi Tsz HoChan Ting FungKwan Kin Ming - : Two novel copper(II) coordination complexes, PH-Cu [(1,10-phenanthroline)(malonato)copper(II)] and PC-Cu [(1,10-phenanthroline)(cyclobutane-1,1-dicarboxylato)copper(II)], were synthesized and evaluated as potential anticancer agents, aiming to characterize structural properties, explore antiproliferative activity and generate mechanistic hypotheses through experimental and computational approaches. : Complexes were characterized by EPR, FTIR-ATR, and ESI-MS, with preliminary SC-XRD data for PH-Cu. Antiproliferative activity was evaluated against six human cancer cell lines using the MTT assay (24 h). Subcellular effects were assessed by fluorescence microscopy and RT-qPCR. Computational studies included DFT geometry optimization, target prediction, molecular docking, and ADMET profiling. : Based on spectroscopic and spectrometric data and comparison with analogous Cu(II) complexes, a distorted square-pyramidal coordination geometry was proposed; this assignment was not confirmed by SC-XRD. Both complexes exhibited potent antiproliferative activity, with PH-Cu showing the highest potency in HeLa cells (IC = 4.22 µM). Under the same conditions, cisplatin showed substantially lower activity (HepG2: 191.1 µM; Caco-2: 129.6 µM; NCI-H69: >333.3 µM; HeLa: 21.9 µM). Fluorescence microscopy at 18 h revealed pyknosis, karyorrhexis, and microtubule disorganization, consistent with regulated cell death. RT-qPCR of PH-Cu indicated intrinsic apoptotic pathway engagement (BAX +3.20-fold; BCL2 to 0.39-fold of control). DFT-optimized bond lengths were consistent with crystallographic data for analogous complexes. Molecular docking suggested PRKCG, RELA (p65), Caspase-3, and α/β-tubulin as interaction candidates, while ADMET profiling predicted favorable intestinal absorption (>92.8%) and low BBB permeability. : These results suggest that the [Cu(phen)] unit constitutes the primary pharmacophore, with the dicarboxylate co-ligand as a modulator of the antiproliferative profile, suggesting promising anticancer pharmacological potential. - Source: PubMed
Publication date: 2026/07/20
García-Díaz Jesús MagdielBacilio-Beltrán Héctor AlejandroGaribaldi-Ríos Asbiel FelipeGallegos-Arreola Martha PatriciaRangel-Salas Irma IdaliaDelgado-Saucedo Jorge IvánCastro-García PaolaMartínez-Velázquez MoisésPuebla-Pérez Ana María - Diabetic foot diseases (DFD) severely impair quality of life, yet specific biomarkers and effective therapies remain limited. Identifying causal molecular targets is critical to address this unmet need. - Source: PubMed
Publication date: 2026/07/21
Fang ManLei YitianFan PengjuWu Hong - Cryptorchidism, among the most frequent congenital urogenital anomalies in male infants, has a global prevalence ranging from 1% to 9%. Characterized by failure of testicular descent into the scrotum, such a condition exposes the testes to elevated temperature, oxidative stress, and impaired spermatogenesis, significantly increasing risks of infertility and testicular cancer. Although orchiopexy is the standard treatment, long-term spermatogenic defects often persist, highlighting the need to elucidate underlying molecular mechanisms. Although the main mechanistic experiments were performed in GC-1 spg cells through genetic manipulation of cPKCγ, an additional heat-stress experiment was included to simulate the high-temperature condition associated with cryptorchidism. In the present study, the role of conventional protein kinase C gamma (cPKCγ) in regulating mitophagy and apoptosis was investigated using mouse spermatogonial GC-1 cells. Through siRNA-mediated knockdown and adenovirus-induced overexpression, cPKCγ upregulation was demonstrated to significantly induce cellular apoptosis and disrupt mitochondrial function, indicated by elevated malondialdehyde (MDA) levels, reduced superoxide dismutase (SOD) activity, decreased ATP production, increased 8-hydroxy-2'-deoxyguanosine (8-OHdG) accumulation, increased mitochondrial reactive oxygen species (ROS), and loss of mitochondrial membrane potential. Mechanistically, cPKCγ was found to inhibit the UCHL1/HIF-1α signaling pathway, suppressing mitophagy, as evidenced by a reduced LC3-II/LC3-I ratio and decreased PINK1 and Parkin expression. Importantly, adverse effects induced by cPKCγ overexpression were substantially rescued through UCHL1 or HIF-1α overexpression, or rapamycin treatment. Conversely, knockdown of UCHL1 or HIF-1α partially counteracted the protective effects of cPKCγ silencing on cell viability, oxidative stress, and mitophagy activation. Furthermore, heat stress upregulated endogenous cPKCγ and suppressed UCHL1/HIF-1α signaling and mitophagy-related proteins in GC-1 spg cells. Collectively, cPKCγ exacerbates spermatogonial apoptosis by repressing UCHL1/HIF-1α-dependent mitophagy, suggesting a potential molecular mechanism for spermatogonial vulnerability under cryptorchidism-related heat stress. - Source: PubMed
Publication date: 2026/07/16
Yang HuajunTian YouFeng ShaoguangShen JingYao XianmingLin Feng - The spinal dorsal horn contains numerous excitatory interneurons, which can be assigned to functional classes based on morphological, electrophysiological and neurochemical criteria. One population consists of neurons that express neurotensin, and these belong to a larger group defined by the presence of protein kinase Cγ (PKCγ). It has been proposed that PKCγ neurons form part of a circuit that can convey low-threshold mechanoreceptive information to nociceptive projection neurons in lamina I, forming a pathway that could underlie mechanical allodynia in pathological pain states. However, despite their potential importance, relatively little is known about the properties of the neurotensin-expressing cells. Here we have used a neurotensin-Cre line, together with intraspinal injection of AAVs coding for Cre-dependent constructs, to characterise the morphological and electrophysiological properties of these cells. Reconstruction of their dendritic trees revealed that they were morphologically diverse, although many could be assigned to a class known as central cells. All cells examined received synaptic contacts from putative A- and C-low-threshold mechanoreceptors (identified by expression of VGLUT1 and VGLUT3, respectively). However, these only accounted for a minority of their excitatory synapses. Around 40% of their synapses were from VGLUT2-immunoreactive boutons, which are likely to have originated mainly from local excitatory interneurons. Electrophysiological analysis revealed similarities to, and differences, from other neurochemically-defined excitatory interneuron populations. Our findings are compatible with the proposed role of neurotensin cells in mechanical allodynia, but suggest additional functions for these cells. - Source: PubMed
Publication date: 2026/07/15
Polgár ErikaDickie Allen CGutierrez-Mecinas MariaWatanabe MasahikoBell Andrew MTodd Andrew J