|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for PRKCH(NM_006255.4) 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.
Validated result:
Summary
Protein kinase C (PKC) is a family of serine- and threonine-specific protein kinases that can be activated by calcium and the 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 family members also serve as major receptors for phorbol esters, a class of tumor promoters. Each member of the PKC family has a specific expression profile and is believed to play a distinct role in cells. The protein encoded by this gene is one of the PKC family members. It is a calcium-independent and phospholipids-dependent protein kinase. It is predominantly expressed in epithelial tissues and has been shown to reside specifically in the cell nucleus. This protein kinase can regulate keratinocyte differentiation by activating the MAP kinase MAPK13 (p38delta)-activated protein kinase cascade that targets CCAAT/enhancer-binding protein alpha (CEBPA). It is also found to mediate the transcription activation of the transglutaminase 1 (TGM1) gene. [provided by RefSeq].
Gene References into function
- that PKC eta negatively regulates UV-induced apoptosis through its localization, resistance to cleavage, and the p38 MAPK pathway
- The novel varepsilon and eta and atypical zeta, but not the conventional alpha and beta and the novel delta PKCs, may be involved in the signaling pathways involved in thrombin-induced human platelet P-selectin expression
- Minute virus of mice infection causes accumulation of endogenous PKCeta in the nuclear periphery and regulaties this NS1 regulating kinase, thus underlining the tight interconnection between PKC-mediated signaling and the parvoviral life cycle
- The major result is a clear correlation of PKC eta expression with tumor progression in renal cell carcinoma.
- There was expression of protein kinase C eta in abnormal muscle fibers. Protein kinase C isoforms may play a role in the pathogenesis of myofibrillar myopathy.
- PKC-eta targets the Akt and mTOR signaling pathways
- These studies demonstrate translocation of PKCeta to the nuclear envelope, and suggest that the spatial regulation of PKCeta could be important for its cellular functions including effects on cell cycle control and involvement in tumor promotion.
- PKC-eta-mediated glioblastoma proliferation involves MEK/mitogen-activated protein (MAP) kinase phosphorylation, activation of ERK and subsequently of Elk-1.
- Our results provide evidence of the involvement of PRKCH as a susceptibility gene for rheumatoid arthritis in the Japanese population
- We report that a nonsynonymous SNP in PRKCH increases the risk of cerebral infarction in the general Japanese population. We also found that PKCeta was expressed in vascular endothelial cells and foamy macrophages in human atherosclerotic lesions.
- Fission of transport carriers at the trans-Golgi network is dependent on specifically PLCbeta3, which is necessary to activate PKCeta and PKD in that Golgi compartment, via diacylglycerol production.
- PKCeta functions as an anti-apoptotic protein in Hodgkin's lymphoma-derived cell lines
- PRKCH mRNA was expressed at lower level in rheumatoid arthritis unrelated patients than in healthy controls, and is not a rheumatoid arthritis major susceptibility genetic factor in the French Caucasian population.
- PRKCH gene polymorphisms have a role in subcortical silent brain infarction
