Anti-Kv3.2

貨號 Cat. No.
APC-011
規格 Size
50 μl 0.2ml

Description

 


Anti-Kv3.2











Product#: APC-011















Sizes:
50 µl
0.2 ml


















Host:
Rabbit














Epitope:

Peptide DLGGKRLGIEDAAGLGGPDGK(C), corresponding to residues 184-204 of rat Kv3.2 (Accession P22462).






















Putative epitope location:
Intracellular, N-terminal part.














Homology:
Human - 19/21 residues identical (based on ESTs).





Applications:










Western Blotting:
 









Western blotting of rat brain membranes:

1.       Anti-Kv3.2 antibody (#APC-011) (1:200).

2.       Anti-Kv3.2 antibody, preincubated with the control peptide antigen.

 















Immunohistochemistry:

Rat brain sections.














References:














1. Rettig, J. et al. (1992) EMBO J 11, 2473.
2. Rudy, B. et al. (1999) Ann NY Acad Sci 868, 304.
3. Rudy, B. et al. (2001) Trends Neurosci. 24, 517.


Kv3.2 is a member of the voltage-gated K+ channel superfamily. Together with the related proteins Kv3.1, Kv3.3 and Kv3.4 they constitute the Shaw type subfamily family.1

 

As with all Kv channels, Kv3.2 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.2,3

 

Kv3.2 is highly expressed in the brain but has been also detected in peripheral organs such as pancreas and mesenteric artery.

 

Kv3.2 and Kv3.1are highly enriched in neurons that fire at high frequencies,such as fast spiking interneurons of the cortex and hippocampusand neurons in the globus pallidus. Their unusuallyrapid activation and deactivation rates allow channels containingKv3.2 and Kv3.1 subunits to repolarize action potentials quickly thus minimizing the rate of recovery of sodium channel inactivation.2,3

 

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