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Gene Ontology Classifications
Symbol
Name
ID
Kcnj10
potassium inwardly-rectifying channel, subfamily J, member 10
MGI:1194504

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

GO curators for mouse genes have assigned the following annotations to the gene product of Kcnj10. (This text reflects annotations as of Thursday, July 24, 2014.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of January 10, 2011. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary from NCBI RefSeq


[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the inward rectifier-type potassium channel family, characterized by having a greater tendency to allow potassium to flow into, rather than out of, a cell. The encoded protein may form a heterodimer with another potassium channel protein and may be responsible for the potassium buffering action of glial cells in the brain. Mutations in this gene have been associated with seizure susceptibility of common idiopathic generalized epilepsy syndromes. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
References
  1. Djukic B et al. (2007) Conditional knock-out of Kir4.1 leads to glial membrane depolarization, inhibition of potassium and glutamate uptake, and enhanced short-term synaptic potentiation. J Neurosci, 27:11354-65. (PubMed:17942730)
  2. Hibino H et al. (2004) Differential assembly of inwardly rectifying K+ channel subunits, Kir4.1 and Kir5.1, in brain astrocytes. J Biol Chem, 279:44065-73. (PubMed:15310750)
  3. Kofuji P et al. (2000) Genetic inactivation of an inwardly rectifying potassium channel (Kir4.1 subunit) in mice: phenotypic impact in retina. J Neurosci, 20:5733-40. (PubMed:10908613)
  4. Kurschner C et al. (1998) CIPP, a novel multivalent PDZ domain protein, selectively interacts with Kir4.0 family members, NMDA receptor subunits, neurexins, and neuroligins. Mol Cell Neurosci, 11:161-72. (PubMed:9647694)
  5. Neusch C et al. (2006) Lack of the Kir4.1 channel subunit abolishes K+ buffering properties of astrocytes in the ventral respiratory group: impact on extracellular K+ regulation. J Neurophysiol, 95:1843-52. (PubMed:16306174)
  6. Reichold M et al. (2010) KCNJ10 gene mutations causing EAST syndrome (epilepsy, ataxia, sensorineural deafness, and tubulopathy) disrupt channel function. Proc Natl Acad Sci U S A, 107:14490-5. (PubMed:20651251)
  7. Seifert G et al. (2009) Analysis of astroglial K+ channel expression in the developing hippocampus reveals a predominant role of the Kir4.1 subunit. J Neurosci, 29:7474-88. (PubMed:19515915)
  8. Tang X et al. (2010) Inwardly rectifying potassium channel Kir4.1 is responsible for the native inward potassium conductance of satellite glial cells in sensory ganglia. Neuroscience, 166:397-407. (PubMed:20074622)
  9. Wu J et al. (2004) Contribution of Kir4.1 to the mouse electroretinogram. Mol Vis, 10:650-4. (PubMed:15359216)
  10. Zhang H et al. (2008) Aquaporin-4 independent Kir4.1 K+ channel function in brain glial cells. Mol Cell Neurosci, 37:1-10. (PubMed:17869537)



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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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last database update
09/09/2014
MGI 5.19
The Jackson Laboratory