Render Target: SSR
Render Timestamp: 2024-12-26T19:18:04.126Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:54:16.374
Product last modified at: 2024-12-17T18:49:05.514Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Kv7.2 (D9L5S) Rabbit mAb #14752

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 95
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    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.

    Species Reactivity:

    Human, Mouse, Rat

    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.

    Background

    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).
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