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Validated All-in-One™ qPCR Primer for PRKCG(NM_001316329.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
Protein kinase C (PKC) is a family of serine- and threonine-specific protein kinases that can be activated by calcium and second messenger diacylglycerol. PKC family members phosphorylate a wide variety of protein targets and are known to be involved in diverse cellular signaling pathways. PKC also serve as major receptors for phorbol esters, a class of tumor promoters.
Gene References into function
- REVIEW:Interaction of protein kinase C isozymes with membranes containing anionic phospholipids utilizing fluorescent phorbol esters to probe the properties of the C1 domains
- Missense mutations occur in the regulatory domain of PKC gamma: a new mechanism for dominant nonepisodic cerebellar ataxia.
- the affinity of isolated C1A and C1B domains of PKCalpha and PKCgamma for soluble and membrane-incorporated DAG and phorbol ester were measured by isothermal calorimetry and surface plasmon resonance in order to compare activation mechanisms
- activation of mGluR5 causes translocation of both gammaPKC and deltaPKC to the plasma membrane. deltaPKC, but not gammaPKC, phosphorylates mGluR5 Thr(840), leading to the blockade of both Ca2+ oscillations and gammaPKC cycling.
- Spinocerebellar ataxia(SCA) type 14 is caused by mutations in PRKCG gene. The observation that all 4 PRKCG mutations identified in patients with SCA to date are located in exon 4 suggests a critical role for this region of the gene in cerebellar function
- We sequenced exons 4 and 5 of PRKCG and detected a missense mutation in exon 4, involving a G-->A transition in nucleotide 353 and resulting in a glycine-to-aspartic acid substitution at residue 118 in a Dutch autosomal dominant cerebellar ataxia family
- osmotic shock in human keratinocytes leads to activation of phospholipase C-gamma1
- spinocerebellar ataxia type 14 mutations make gammaPKC form cytoplasmic aggregates, which may play a role in development of SCA14
- Six mutations were found that segregated with the disease including F643L (exon 18), Five new missense mutations were identified in exons 4 (C114Y/G123R/G123E), 10 (G360S) and 18 (V692G).
- These results indicate that PKCgamma regulates NMHC-IIB phosphorylation and cellular localization in response to EGF stimulation.
- These results suggest that the PKC gamma R659S mutation is susceptible to neuronal death and is involved in the pathogenesis of neurodegenerative diseases, including Retinitis pigmentosa.
- The present findings show that the interaction between PKCgamma and GluR4 is specifically required to assure PKC-driven phosphorylation and surface membrane expression of GluR4.
- PRKCG mutation (SCA-14) causing a Ramsay Hunt phenotype.
- detection of a new mutation in PRKCG responsible for spinocerebellar ataxia type 14, which may be located in a mutational hot spot
- Codon 101 of PRKCG, a preferential mutation site in SCA14.
- This study present a benign SCA14 phenotype in a German patient associated with a missense mutation in exon 3 of the PRKCG gene
- PKCgamma, but not C1 domain mutants, inhibits Ca2+ influx in response to muscarinic receptor stimulation.
- These studies suggest that Purkinje cell damage in SCA14 may result from a reduction of PKCgamma activity due its aberrant sequestration in the early endosome compartment.
- The impact of three C1B regulatory subdomain mutations on the intracellular kinetics, protein conformation and kinase activity of PKCgamma in living cells, was investigated.
- Rac regulates the interaction of fascin with active PKC.
- study investigated whether mutant gammaPKC formed aggregates and how mutant gammaPKC affects the morphology and survival of cerebellar Purkinje cells (PCs), which are degenerated in SCA14 patients
- Using shotgun mass spectrometry, we found this protein differentially expressed in the dorsolateral prefrontal cortex from patients with schizophrenia.
