KCNN1
From Wikipedia, the free encyclopedia
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Potassium intermediate/small conductance calcium-activated channel, subfamily N, member 1
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| Identifiers | ||||||||||||||
| Symbol(s) | KCNN1; KCa2.1; SK1; SKCA1; hSK1 | |||||||||||||
| External IDs | OMIM: 602982 MGI: 1933993 HomoloGene: 37595 | |||||||||||||
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| RNA expression pattern | ||||||||||||||
| Orthologs | ||||||||||||||
| Human | Mouse | |||||||||||||
| Entrez | 3780 | 84036 | ||||||||||||
| Ensembl | ENSG00000105642 | ENSMUSG00000002908 | ||||||||||||
| Uniprot | Q92952 | Q9EQR3 | ||||||||||||
| Refseq | NM_002248 (mRNA) NP_002239 (protein) |
NM_032397 (mRNA) NP_115773 (protein) |
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| Location | Chr 19: 17.95 - 17.97 Mb | Chr 8: 73.77 - 73.78 Mb | ||||||||||||
| Pubmed search | [1] | [2] | ||||||||||||
Potassium intermediate/small conductance calcium-activated channel, subfamily N, member 1, also known as KCNN1, is a human gene.[1]
Action potentials in vertebrate neurons are followed by an afterhyperpolarization (AHP) that may persist for several seconds and may have profound consequences for the firing pattern of the neuron. Each component of the AHP is kinetically distinct and is mediated by different calcium-activated potassium channels. The protein encoded by this gene is activated before membrane hyperpolarization and is thought to regulate neuronal excitability by contributing to the slow component of synaptic AHP. The encoded protein is an integral membrane protein that forms a voltage-independent calcium-activated channel with three other calmodulin-binding subunits. This gene is a member of the KCNN family of potassium channel genes.[1]
[edit] See also
[edit] References
[edit] Further reading
- Wei AD, Gutman GA, Aldrich R, et al. (2006). "International Union of Pharmacology. LII. Nomenclature and molecular relationships of calcium-activated potassium channels.". Pharmacol. Rev. 57 (4): 463–72. doi:. PMID 16382103.
- Köhler M, Hirschberg B, Bond CT, et al. (1996). "Small-conductance, calcium-activated potassium channels from mammalian brain.". Science 273 (5282): 1709–14. PMID 8781233.
- Litt M, LaMorticella D, Bond CT, Adelman JP (1999). "Gene structure and chromosome mapping of the human small-conductance calcium-activated potassium channel SK1 gene (KCNN1).". Cytogenet. Cell Genet. 86 (1): 70–3. PMID 10516439.
- Shah M, Haylett DG (2000). "The pharmacology of hSK1 Ca2+-activated K+ channels expressed in mammalian cell lines.". Br. J. Pharmacol. 129 (4): 627–30. doi:. PMID 10683185.
- Liu QH, Williams DA, McManus C, et al. (2000). "HIV-1 gp120 and chemokines activate ion channels in primary macrophages through CCR5 and CXCR4 stimulation.". Proc. Natl. Acad. Sci. U.S.A. 97 (9): 4832–7. doi:. PMID 10758170.
- Rimini R, Rimland JM, Terstappen GC (2001). "Quantitative expression analysis of the small conductance calcium-activated potassium channels, SK1, SK2 and SK3, in human brain.". Brain Res. Mol. Brain Res. 85 (1-2): 218–20. PMID 11146124.
- Zhang BM, Kohli V, Adachi R, et al. (2001). "Calmodulin binding to the C-terminus of the small-conductance Ca2+-activated K+ channel hSK1 is affected by alternative splicing.". Biochemistry 40 (10): 3189–95. PMID 11258935.
- Boettger MK, Till S, Chen MX, et al. (2002). "Calcium-activated potassium channel SK1- and IK1-like immunoreactivity in injured human sensory neurones and its regulation by neurotrophic factors.". Brain 125 (Pt 2): 252–63. PMID 11844726.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:. PMID 12477932.
- Arnold SJ, Facer P, Yiangou Y, et al. (2003). "Decreased potassium channel IK1 and its regulator neurotrophin-3 (NT-3) in inflamed human bowel.". Neuroreport 14 (2): 191–5. doi:. PMID 12598727.
- Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).". Genome Res. 14 (10B): 2121–7. doi:. PMID 15489334.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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