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Gene Ontology Classifications
potassium large conductance calcium-activated channel, subfamily M, alpha member 1

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

GO curators for mouse genes have assigned the following annotations to the gene product of Kcnma1. (This text reflects annotations as of Tuesday, May 26, 2015.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of July 3, 2007. 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.] MaxiK channels are large conductance, voltage and calcium-sensitive potassium channels which are fundamental to the control of smooth muscle tone and neuronal excitability. MaxiK channels can be formed by 2 subunits: the pore-forming alpha subunit, which is the product of this gene, and the modulatory beta subunit. Intracellular calcium regulates the physical association between the alpha and beta subunits. Alternatively spliced transcript variants encoding different isoforms have been identified. [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
  1. Butler A et al. (1993) mSlo, a complex mouse gene encoding maxi calcium-activated potassium channels. Science, 261:221-4. (PubMed:7687074)
  2. Chen L et al. (2005) Functionally diverse complement of large conductance calcium- and voltage-activated potassium channel (BK) alpha-subunits generated from a single site of splicing. J Biol Chem, 280:33599-609. (PubMed:16081418)
  3. Eghbali M et al. (2003) Diminished surface clustering and increased perinuclear accumulation of large conductance Ca2+-activated K+ channel in mouse myometrium with pregnancy. J Biol Chem, 278:45311-7. (PubMed:12952984)
  4. Engel J et al. (2006) Two classes of outer hair cells along the tonotopic axis of the cochlea. Neuroscience, 143:837-49. (PubMed:17074442)
  5. Jha S et al. (2009) The beta1 subunit of Na+/K+-ATPase interacts with BKCa channels and affects their steady-state expression on the cell surface. FEBS Lett, 583:3109-14. (PubMed:19729011)
  6. Kathiresan T et al. (2009) A protein interaction network for the large conductance Ca2+-activated K+ channel in the mouse cochlea. Mol Cell Proteomics, null:null. (PubMed:19423573)
  7. Ma D et al. (2007) Differential trafficking of carboxyl isoforms of Ca(2+)-gated (Slo1) potassium channels. FEBS Lett, 581:1000-8. (PubMed:17303127)
  8. McCartney CE et al. (2005) A cysteine-rich motif confers hypoxia sensitivity to mammalian large conductance voltage- and Ca-activated K (BK) channel alpha-subunits. Proc Natl Acad Sci U S A, 102:17870-6. (PubMed:16306267)
  9. Meredith AL et al. (2006) BK calcium-activated potassium channels regulate circadian behavioral rhythms and pacemaker output. Nat Neurosci, 9:1041-1049. (PubMed:16845385)
  10. Meredith AL et al. (2004) Overactive bladder and incontinence in the absence of the BK large conductance Ca2+-activated K+ channel. J Biol Chem, 279:36746-52. (PubMed:15184377)
  11. Nagai T et al. (2006) The rewards of nicotine: regulation by tissue plasminogen activator-plasmin system through protease activated receptor-1. J Neurosci, 26:12374-83. (PubMed:17122062)
  12. Nehrke K et al. (2003) Molecular identification of Ca2+-activated K+ channels in parotid acinar cells. Am J Physiol Cell Physiol, 284:C535-46. (PubMed:12388098)
  13. Oliver D et al. (2006) The role of BKCa channels in electrical signal encoding in the mammalian auditory periphery. J Neurosci, 26:6181-9. (PubMed:16763026)
  14. Pan NC et al. (2014) Activation of galanin receptor 2 stimulates large conductance Ca(2+)-dependent K(+) (BK) channels through the IP3 pathway in human embryonic kidney (HEK293) cells. Biochem Biophys Res Commun, 446:316-21. (PubMed:24602615)
  15. Pyott SJ et al. (2007) Cochlear function in mice lacking the BK channel alpha, beta1, or beta4 subunits. J Biol Chem, 282:3312-24. (PubMed:17135251)
  16. Romanenko V et al. (2006) Molecular identification and physiological roles of parotid acinar cell maxi-K channels. J Biol Chem, 281:27964-72. (PubMed:16873365)
  17. Ruttiger L et al. (2004) Deletion of the Ca2+-activated potassium (BK) alpha-subunit but not the BKbeta1-subunit leads to progressive hearing loss. Proc Natl Acad Sci U S A, 101:12922-7. (PubMed:15328414)
  18. Sausbier M et al. (2005) Elevated blood pressure linked to primary hyperaldosteronism and impaired vasodilation in BK channel-deficient mice. Circulation, 112:60-8. (PubMed:15867178)
  19. Sausbier M et al. (2004) Cerebellar ataxia and Purkinje cell dysfunction caused by Ca2+-activated K+ channel deficiency. Proc Natl Acad Sci U S A, 101:9474-8. (PubMed:15194823)
  20. Shipston MJ et al. (1999) Molecular components of large conductance calcium-activated potassium (BK) channels in mouse pituitary corticotropes. Mol Endocrinol, 13:1728-37. (PubMed:10517674)
  21. Thorneloe KS et al. (2005) Urodynamic properties and neurotransmitter dependence of urinary bladder contractility in the BK channel deletion model of overactive bladder. Am J Physiol Renal Physiol, 289:F604-10. (PubMed:15827347)
  22. Tian L et al. (2006) A noncanonical SH3 domain binding motif links BK channels to the actin cytoskeleton via the SH3 adapter cortactin. FASEB J, 20:2588-90. (PubMed:17065230)

Go Annotations in Tabular Form (Text View) (GO Graph)

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Gene Ontology Evidence Code Abbreviations:

  EXP Inferred from experiment
  IAS Inferred from ancestral sequence
  IBA Inferred from biological aspect of ancestor
  IBD Inferred from biological aspect of descendant
  IC Inferred by curator
  IDA Inferred from direct assay
  IEA Inferred from electronic annotation
  IGI Inferred from genetic interaction
  IKR Inferred from key residues
  IMP Inferred from mutant phenotype
  IMR Inferred from missing residues
  IPI Inferred from physical interaction
  IRD Inferred from rapid divergence
  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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