Anti-Kv7.2 (KCNQ2)

貨號 Cat. No.
APC-050
規格 Size
50 μl 0.2ml

Description

Anti-Kv7.2 (KCNQ2)












Product#: APC-050



























Sizes:
50 ml
0.2 ml
 
 
 
 





The KCNQ family of voltage-gated K+ channels includes 5 known members: KCNQ1 to KCNQ5.  

Structurally, the KCNQ family belongs to the six transmembrane domain category of K+ channels.  

KCNQ family members can form either homomultimeric or heteromultimeric channels with different  

functional consequences. For example KCNQ2 and KCNQ3 heteromultimers give rise to a much  

larger channel current than when either protein is expressed alone, probably due to enhanced  

plasma membrane expression of the combined channel. Indeed, KCNQ2/KCNQ3 heteromultimers are  

believed to be the molecular correlates of the so-called M current. This current is a K+ neuronal current  

that is strongly inhibited by the activation of the M1 subtype of the muscarinic acetylcholine receptor.  

Mutations in either KCNQ2 or KCNQ3 are associated with a form of epilepsy known as benign familial  

neonatal convulsions (BNFC).
















Host:
Rabbit.








 










Epitope:
Peptide (C)RGPTITDKDRTKGPAE, corresponding to amino acid residues 578-593 of rat KCNQ2 (Accession number O88943).








 







 










Putative epitope location:
Intracellular, C-terminal domain.







 










Homology:

Mouse ?identical; human- 15/16 residues identical.


Specificity:  

The antibody is specific for KCNQ2; it does not cross react with KCNQ3 or other QKT proteins. 

There are at least 9 recognized splice variants of rat KCNQ2.  This antibody recognizes all except splice variants B and C. 









 










Reactivity Confirmed:
Rat.








 

Applications:










Western Blotting:
Kv7.2 transfected HEK-293 cells (1:200).











Western blotting of Kv7.2 transfected HEK-293 cells:  

1. Anti-Kv7.2 antibody (1:200).   

2. Anti-Kv7.2, preincubated with the control peptide antigen.







 

Control antigen included in price









References:


















1.


Kullmann, D.M. (2002) J. Mol. Brain 125, 1117.  


2.


Robbins, J. (2001) Pharmacol. Ther. 90, 1.  


3.


Wang, H.S. et al. (1998) Science 282, 1890.  


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