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This review showed that the PKC Gamma signaling related genes and calcium signaling related genes then discuss their role for both Purkinje cell dendritic development and cerebellar ataxia.
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SUMOylation of EphB1 repressed activation of its downstream signaling molecule PKC-gamma, and consequently inhibited neuroblastoma tumorigenesis.
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two out of three known mutations in the catalytic domain of PKCgamma did indeed show increased biological activity.
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Lysophosphatidylcholines prime polymorphonuclear neutrophil through Hck-dependent activation of PKCdelta, which stimulates PKCgamma, resulting in translocation of phosphorylated p47(phox).
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The gene-environment combination of PRKCG rs3745406 C allele, BDNF rs6265 G allele and high level of negative life events was significantly associated with major depressive disorder.
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The results showed that carrier of rs454006*C allele and rs3745406*C might elevate the risk of osteosarcoma
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Data suggest that PRKCG (protein kinase C gamma) phosphorylates TA isoforms of p63 (tumor protein p63) at Thr157 to stabilize them and promote cell apoptosis in tumor cells.
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PKCgamma,mutated in the neurodegenerative disease spinocerebellar ataxia type 14 is a novel amyloidogenic protein.
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The rs454006 polymorphism of the PRKCG gene correlated to osteosarcoma susceptibility and might increase the risk of osteosarcoma.
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findings provide evidence for both an increased PKCgamma activity in Purkinje cells in vivo and for pathological changes typical for cerebellar disease thus linking increased and dysregulated activity of PKCgamma to development of cerebellar disease
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we show that the mutation V138E of the protein kinase C gamma (PKCgamma) C1B domain, which is implicated in spinocerebellar ataxia type 14, exhibits a partially unfolded C-terminus
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PKCgamma plays a critical role in cancer cells, and simultaneous inhibition of PKCgamma and Hsp90alpha synergistically prevents cell migration and promotes apoptosis in cancer cells.
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A novel missense mutation, F643L, which maps to a highly conserved amino acid of the catalytic domain of protein kinase C gamma, extends the phenotype associated with the spinocerebellar ataxia type 14 (SCA14) locus.
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Spinocerebellar ataxia type 14 mutant PKC-gamma upregulates Hsp70. Hsp70 has a role in degrading mutant PKC-gamma.
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Exome sequencing of large, 5-generational British kindred finds a novel p.Arg26Gly mutation in the PRKCG gene causing familial spinocerebellar ataxia 14.
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SCA14, a novel mutation in the PRKCG gene, was found in two families in Norway with autosomal dominant cerebellar ataxia.
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We propose that variety of mutant gammaPKC characters integrally and complicatedly participate in the pathophysiology of SCA 14.
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The Spinocerebellar ataxia type 14 is caused by mutations in the protein kinase C gamma (PKCgamma, PRKCG) gene with a hotspot for mutations in exon 4. Genetic testing for SCA14 is clinically available.
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Data show that through HINT1, the MOR facilitates the cross-talk of two NO- and zinc-regulated signal-transduction pathways, PKC/Src and Raf-1/ERK1/2, implicated in the negative control of morphine effects.
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cPLA(2)-dependent AA release is required for VEGF-induced Src-PLD1-PKCgamma-mediated pathological retinal angiogenesis
