Biology:CACNA1G

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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

Calcium channel, voltage-dependent, T type, alpha 1G subunit, also known as CACNA1G or Cav3.1 is a protein which in humans is encoded by the CACNA1G gene.[1][2][3] It is one of the primary targets in the pharmacology of absence seizure.

Function

Cav3.1 is a type of low-voltage-activated calcium channel, also known as "T-type" for its transient on and off.[1] It is expressed in thalamocortical relay nucleus, and is responsible for the slow-wave sleep and absence seizure.[4] During a slow-wave sleep, Cav3.1 is put into burst mode, and a self-sustaining synchronous cycle between cortex and thalamus is formed, sensory inputs are isolated from cortex; while awake the thalamus should instead relay sensory inputs from outside the central nervous system. The mechanism of absence seizure has a lot in common with slow-wave sleep. Therefore, a blocker that inhibits the burst mode activation of Cav3.1 is effective in treating absence seizures. Common drugs including ethosuximide, as well as trimethadione.[4]


Interactive pathway map

See also

References

  1. 1.0 1.1 "Entrez Gene: CACNA1H calcium channel, voltage-dependent, T type, alpha 1H subunit". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=8913. 
  2. "Molecular characterization of a neuronal low-voltage-activated T-type calcium channel". Nature 391 (6670): 896–900. February 1998. doi:10.1038/36110. PMID 9495342. Bibcode1998Natur.391..896P. 
  3. "International Union of Pharmacology. XLVIII. Nomenclature and structure-function relationships of voltage-gated calcium channels". Pharmacol. Rev. 57 (4): 411–25. December 2005. doi:10.1124/pr.57.4.5. PMID 16382099. 
  4. 4.0 4.1 Kopecky, Benjamin J.; Liang, Ruqiang; Bao, Jianxin (2014). "T-type Calcium Channel Blockers as Neuroprotective Agents". Pflügers Archiv 466 (4): 757–765. doi:10.1007/s00424-014-1454-x. ISSN 0031-6768. PMID 24563219. 

External links

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