Kcnc1 Rabbit Polyclonal Antibody

Specifications

Product Data
Applications	WB
Recommend Dilution	WB: 1:200-1:2000; IHC: 1:100-1:3000
Reactivity	Mouse, Rat
Host	Rabbit
Clonality	Polyclonal
Immunogen	Peptide CKESPVIAKYMPTEAVRVT, corresponding to amino acid residues 567-585 of rat Kv3.1b .? ? Intracellular, C-terminus.
Formulation	Lyophilized. Concentration before lyophilization ~0.8mg/ml (lot dependent, please refer to CoA along with shipment for actual concentration). Buffer before lyophilization: phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.05% NaN3.
Reconstitution Method	Add 50 ul double distilled water (DDW) to the lyophilized powder.
Purification	Affinity purified on immobilized peptide.
Conjugation	Unconjugated
Storage Condition	Store at -20°C as received.
Gene Name	potassium voltage-gated channel subfamily C member 1
Database Link	NP_036988 Entrez Gene 16502 MouseEntrez Gene 25327 Rat UniProt ID P25122
Background	KV3.1 is a member of the voltage-gated K+ channel superfamily. Together with the related proteins KV3.2, KV3.3 and KV3.4 they constitute the Shaw type subfamily family. As with all KV channels, KV3.1 possesses the signature structure of the voltage-dependent K+ channels: six membrane-spanning domains with intracellular N and C termini. The functional Kv channel is a tetramer that can either be a homomer or a heteromer of KV3 subunits. KV3 subfamily members inactivate very rapidly and therefore are thought to play a role in the repolarization of action potentials and to facilitate repetitive high frequency firing. KV3.1 is highly expressed in the brain but has been also detected in peripheral organs such as lung skeletal muscle and testis. KV3.1 and KV3.2 are highly enriched in neurons that fire at high frequencies, such as fast spiking interneurons of the cortex and hippocampus and neurons in the globus pallidus. Their unusually rapid activation and deactivation rates allow channels containing KV3.1 and KV3.2 subunits to repolarize action potentials quickly thus minimizing the rate of recovery of sodium channel inactivation. Lack of KV3.1 channel subunits is mainly responsible for constitutively increased locomotor activity and sleep loss.
Synonyms	FLJ41162; FLJ42249; FLJ43491; Kv3.1; KV4; MGC129855; NGK2
Reference Data

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