Biology:KCNS3

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Short description: Protein-coding gene in the species Homo sapiens


A representation of the 3D structure of the protein myoglobin showing turquoise α-helices.
Generic protein structure example

Potassium voltage-gated channel subfamily S member 3 (Kv9.3) is a protein that in humans is encoded by the KCNS3 gene.[1][2][3] KCNS3 gene belongs to the S subfamily of the potassium channel family.[3] It is highly expressed in pulmonary artery myocytes,[4][5][6] placenta,[7] and parvalbumin-containing GABA neurons in brain cortex.[8][9] In humans, single-nucleotide polymorphisms of the KCNS3 gene are associated with airway hyperresponsiveness,[10] whereas decreased KCNS3 mRNA expression is found in the prefrontal cortex of patients with schizophrenia.[9]

Function

Voltage-gated potassium channels form the largest and most diversified class of ion channels and are present in both excitable and nonexcitable cells. Their main functions are associated with the regulation of the resting membrane potential and the control of the shape and frequency of action potentials. The alpha subunits are of 2 types: those that are functional by themselves and those that are electrically silent but capable of modulating the activity of specific functional alpha subunits. The Kv9.3 protein (encoded by KCNS3 gene) is not functional by itself[5] but can form functional heteromultimers with Kv2.1 (encoded by KCNB1) and Kv2.2 (encoded by KCNB2) (and possibly other members) of the Shab-related subfamily of potassium voltage-gated channel proteins.[4] Heteromeric Kv2.1/Kv9.3 channels form with fixed stoichiometry consisting of three Kv2.1 subunits and one Kv9.3 subunit.[11]

See also

References

  1. "Electrically silent potassium channel subunits from human lens epithelium". The American Journal of Physiology 277 (3): C412–C424. September 1999. doi:10.1152/ajpcell.1999.277.3.C412. PMID 10484328. 
  2. "International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage-gated potassium channels". Pharmacological Reviews 57 (4): 473–508. December 2005. doi:10.1124/pr.57.4.10. PMID 16382104. 
  3. 3.0 3.1 "Entrez Gene: KCNS3 potassium voltage-gated channel, delayed-rectifier, subfamily S, member 3". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3790. 
  4. 4.0 4.1 "Kv2.1/Kv9.3, a novel ATP-dependent delayed-rectifier K+ channel in oxygen-sensitive pulmonary artery myocytes". The EMBO Journal 16 (22): 6615–6625. November 1997. doi:10.1093/emboj/16.22.6615. PMID 9362476. 
  5. 5.0 5.1 "Cloning and tissue distribution of two new potassium channel alpha-subunits from rat brain". Biochemical and Biophysical Research Communications 248 (3): 927–934. July 1998. doi:10.1006/bbrc.1998.9072. PMID 9704029. 
  6. "Bone morphogenetic protein-2 upregulates expression and function of voltage-gated K+ channels in human pulmonary artery smooth muscle cells". American Journal of Physiology. Lung Cellular and Molecular Physiology 291 (5): L993-1004. November 2006. doi:10.1152/ajplung.00191.2005. PMID 16815889. 
  7. "Expression of an electrically silent voltage-gated potassium channel in the human placenta". Journal of Obstetrics and Gynaecology 32 (7): 624–629. October 2012. doi:10.3109/01443615.2012.709288. PMID 22943705. 
  8. "Selective expression of KCNS3 potassium channel α-subunit in parvalbumin-containing GABA neurons in the human prefrontal cortex". PLOS ONE 7 (8): e43904. 2012. doi:10.1371/journal.pone.0043904. PMID 22937123. Bibcode2012PLoSO...743904G. 
  9. 9.0 9.1 "Lower gene expression for KCNS3 potassium channel subunit in parvalbumin-containing neurons in the prefrontal cortex in schizophrenia". The American Journal of Psychiatry 171 (1): 62–71. January 2014. doi:10.1176/appi.ajp.2013.13040468. PMID 24170294. 
  10. "Single-nucleotide polymorphisms of the KCNS3 gene are significantly associated with airway hyperresponsiveness". Human Genetics 116 (5): 378–383. April 2005. doi:10.1007/s00439-005-1256-5. PMID 15714333. 
  11. "Fluorescence measurements reveal stoichiometry of K+ channels formed by modulatory and delayed rectifier alpha-subunits". Proceedings of the National Academy of Sciences of the United States of America 102 (17): 6160–6165. April 2005. doi:10.1073/pnas.0500468102. PMID 15827117. Bibcode2005PNAS..102.6160K. 

This article incorporates text from the United States National Library of Medicine, which is in the public domain.