Cell Signaling Technology

Product Pathways - Neuroscience

Kv7.2 (D9L5S) Rabbit mAb #14752

No. Size Price
14752S 100 µl ( 10 western blots ) ¥3,250.00 现货查询 购买询价 防伪查询
14752 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat, Endogenous 95 Rabbit IgG
IP 1:50

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Specificity / Sensitivity

Kv7.2 (D9L5S) Rabbit mAb recognizes endogenous levels of total Kv7.2 protein. This antibody does not cross-react with Kv7.3 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human Kv7.2 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse and rat brain membrane using Kv7.2 (D9L5S) Rabbit mAb.



Immunoprecipitation of Kv7.2 from mouse brain membrane extracts using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2) or Kv7.2 (D9L5S) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Kv7.2 (D9L5S) Rabbit mAb.


The voltage gated potassium channel Kv7.2 (KCNQ2) associates with its family member Kv7.3 (KCNQ3) to form an M-channel that is involved in synaptic input response and sub-threshold excitability of neurons (1). This heteromeric channel generates the M-current, a slowly activating and deactivating potassium conductance that determines the neuronal excitability (2,3). Expression of these two M-channel proteins is mainly seen within the central nervous system, with both Kv7.2 and Kv7.3 expressed post-synaptically in the human cortex and hippocampus (4). The calcium-binding protein calmodulin binds two separate sites in Kv7.2 to influence exit of the channel protein from the endoplasmic reticulum and translocation to the plasma membrane (5). Mutations in the corresponding KCNQ2 gene cause benign familial neonatal seizures-1 (BFNS1), an autosomal dominant form of epilepsy characterized by seizure clusters closely following birth (6,7).

  1. Stewart, A.P. et al. (2012) J Biol Chem 287, 11870-7.
  2. Wang, H.S. et al. (1998) Science 282, 1890-3.
  3. Smith, J.S. et al. (2001) J Neurosci 21, 1096-103.
  4. Cooper, E.C. et al. (2000) Proc Natl Acad Sci U S A 97, 4914-9.
  5. Alaimo, A. et al. (2013) J Cell Sci 126, 244-53.
  6. Miraglia del Giudice, E. et al. (2000) Eur J Hum Genet 8, 994-7.
  7. Dedek, K. et al. (2001) Proc Natl Acad Sci U S A 98, 12272-7.

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