Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Prkcg. (This text reflects annotations as of Wednesday, January 23, 2013.)

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] 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. Each member of the PKC family has a specific expression profile and is believed to play distinct roles in cells. The protein encoded by this gene is one of the PKC family members. This protein kinase is expressed solely in the brain and spinal cord and its localization is restricted to neurons. It has been demonstrated that several neuronal functions, including long term potentiation (LTP) and long term depression (LTD), specifically require this kinase. Knockout studies in mice also suggest that this kinase may be involved in neuropathic pain development. Defects in this protein have been associated with neurodegenerative disorder spinocerebellar ataxia-14 (SCA14). [provided by RefSeq, Jul 2008]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Prkcg
  • is located in the following cellular components:
    • cytoplasm ^{[3, 4, 8, 9]}
    • dendrite ^[9]
    • nucleus ^{[3, 8]}
    • plasma membrane ^{[4, 8]}
    • synaptic membrane ^[6]
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Prkcg
  • participates in the following biological processes:
    • chemosensory behavior ^[1]
    • innervation ^[2]
    • response to morphine ^[7]
    • response to pain ^[5]
    • synaptic transmission ^[2]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Prkcg:
  • participates in the following biological processes:
    • negative regulation of neuron apoptotic process
    • negative regulation of protein catabolic process
    • negative regulation of protein ubiquitination
    • phosphorylation
    • positive regulation of mismatch repair
    • protein autophosphorylation
    • response to stress
  • performs the following molecular functions:
    • calcium-dependent protein kinase C activity
    • protein kinase activity
    • protein kinase C activity
  • is located in the following cellular components:
    • cytosol
    • dendrite
    • neuron projection
    • perinuclear region of cytoplasm
    • plasma membrane

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Summary text based on GO annotations supported by structural data

• Prkcg encodes a protein or proteins that contain the following InterPro domains: AGC-kinase, C-terminal, C2 calcium-dependent membrane targeting, C2 calcium/lipid-binding domain, CaLB, C2 domain, C2 membrane targeting protein, Diacylglycerol/phorbol-ester binding, Protein kinase C, alpha/beta/gamma types, Protein kinase C-like, phorbol ester/diacylglycerol binding, Protein kinase, ATP binding site, Protein kinase, C-terminal, Protein kinase, catalytic domain, Protein kinase-like domain, Serine/threonine- / dual-specificity protein kinase, catalytic domain, Serine/threonine-protein kinase, active site, indicating that the gene product:
  • participates in the following biological processes:
    • intracellular signal transduction
    • protein phosphorylation
  • performs the following molecular functions:
    • ATP binding
    • protein serine/threonine kinase activity
    • transferase activity, transferring phosphorus-containing groups
    • zinc ion binding

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Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Prkcg indicates that it:
  • performs the following molecular functions:
    • ATP binding
    • kinase activity
    • metal ion binding
    • nucleotide binding
    • protein serine/threonine kinase activity
    • transferase activity
  • is located in the following cellular components:
    • cell junction
    • cell projection
    • membrane
    • synapse

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References

1. Bowers BJ et al. (2001) Ethanol consumption and behavioral impulsivity are increased in protein kinase Cgamma null mutant mice. J Neurosci, 21:RC180. (PubMed:11606660)
2. Chen C et al. (1995) Impaired motor coordination correlates with persistent multiple climbing fiber innervation in PKC gamma mutant mice. Cell, 83:1233-42. (PubMed:8548809)
3. Cogram P et al. (2004) Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. Hum Mol Genet, 13:7-14. (PubMed:14613966)
4. Ikeda A et al. (2007) Abnormal features in mutant cerebellar Purkinje cells lacking junctophilins. Biochem Biophys Res Commun, 363:835-9. (PubMed:17904530)
5. Malmberg AB et al. (1997) Preserved acute pain and reduced neuropathic pain in mice lacking PKCgamma [see comments] Science, 278:279-83. (PubMed:9323205)
6. Matsumoto S et al. (2008) Isoflurane inhibits protein kinase Cgamma and calcium/calmodulin dependent protein kinase ii-alpha translocation to synaptic membranes in ischemic mice brains. Neurochem Res, 33:2302-9. (PubMed:18473171)
7. Narita M et al. (2001) Involvement of protein kinase Cgamma isoform in morphine-induced reinforcing effects. Neuroscience, 103:309-14. (PubMed:11246146)
8. Pauken CM et al. (2000) The expression and stage-specific localization of protein kinase C isotypes during mouse preimplantation development. Dev Biol, 223:411-21. (PubMed:10882525)
9. Skinner PJ et al. (2001) Altered trafficking of membrane proteins in purkinje cells of SCA1 transgenic mice. Am J Pathol, 159:905-13. (PubMed:11549583)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

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