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CACNA1G
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CACNA1G
Identifiers
AliasesCACNA1G, Ca(V)T.1, Cav3.1, NBR13, SCA42, calcium voltage-gated channel subunit alpha1 G, SCA42ND
External IDsOMIM: 604065; MGI: 1201678; HomoloGene: 22544; GeneCards: CACNA1G; OMA:CACNA1G - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001112813
NM_001177888
NM_001177890
NM_009783

RefSeq (protein)

n/a

Location (UCSC)Chr 17: 50.56 – 50.63 MbChr 11: 94.3 – 94.37 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

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.[5][6][7] It is one of the primary targets in the pharmacology of absence seizure.

Function

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Cav3.1 is a type of low-voltage-activated calcium channel, also known as "T-type" for its transient on and off.[5] It is expressed in thalamocortical relay nucleus, and is responsible for the slow-wave sleep and absence seizure.[8] 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.[8]


Interactive pathway map

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Click on genes, proteins and metabolites below to link to respective Wikipedia articles. [§ 1]

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NicotineActivityonChromaffinCells_WP1603Go to articlego to articleGo to articleGo to articleGo to articleGo to articlego to articlego to articleGo to articleGo to articlego to articleGo to articleGo to article
|alt=Nicotine Activity on Chromaffin Cells edit]]
Nicotine Activity on Chromaffin Cells edit
  1. ^ The interactive pathway map can be edited at WikiPathways: "NicotineActivityonChromaffinCells_WP1603".

See also

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References

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