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CACNA1G Recombinant Mouse Monoclonal Antibody [PSH23-59] (HA601604)

Price: Regular price $385.00

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Catalog# HA601604

Mouse Monoclonal to CACNA1G

Tested for

  • WB

  • IHC-P

Reacts with

  • Mouse

  • Rat

Recombinant production enables lot-to-lot consistency and is animal-cruelty-free

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Specifications

Product Type

Recombinant Mouse monoclonal primary

Product Name

CACNA1G Recombinant Mouse Monoclonal Antibody [PSH23-59] (HA601604)

Host

Mouse

Positive Control

Rat brain tissue lysates.

Conjugation

Unconjugated

Clonality

Monoclonal

Clone Number

PSH23-59

APPLICATION DILUTION

  • WB

  • 1:2,000

  • IHC-P

  • 1:200

PROPERTIES

Form

Liquid

Storage Condition

Shipped at 4℃. Store at +4℃ short term (1-2 weeks). It is recommended to aliquot into single-use upon delivery. Store at -20℃ long term.

Storage Buffer

1*PBS (pH7.4), 0.1% BSA, 40% Glycerol, 0.2% Proclean 950.

Concentration

1ug/ul

Purification

Protein A affinity purified.

Molecular Weight

Predicted band size: 250 kDa

Isotype

IgG1

TARGET

UNIPROT #

Q9WUT2

PROTEIN NAME

CACNA1G

SYNONYMS

Voltage-dependent T-type calcium channel subunit alpha-1G;Voltage-gated calcium channel subunit alpha Cav3.1;Cacna1g

SUBCELLULAR LOCATION

Cell membrane, Cytoplasm.

FUNCTION

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

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