KCNQ4, Blocking Peptide

For Research Use Only. Not for use in diagnostic procedures.

Lyophilized powder

Add 100ul of sterile PBS. Final peptide concentration is 1 mg/ml in PBS. For longer periods of storage, store at -20 degree C. Avoid repeat freeze-thaw cycles.

Small volumes of KCNQ4 blocking peptide vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

This is a synthetic peptide designed for use in combination with anti-KCNQ4 Antibody, made

Target Description: The protein encoded by this gene forms a potassium channel that is thought to play a critical role in the regulation of neuronal excitability, particularly in sensory cells of the cochlea. The current generated by this channel is inhibited by M1 muscarinic acetylcholine receptors and activated by retigabine, a novel anti-convulsant drug. The encoded protein can form a homomultimeric potassium channel or possibly a heteromultimeric channel in association with the protein encoded by the KCNQ3 gene. Defects in this gene are a cause of nonsyndromic sensorineural deafness type 2 (DFNA2), an autosomal dominant form of progressive hearing loss. Two transcript variants encoding different isoforms have been found for this gene.

Peptide

Western Blot (WB)

76 kDa

potassium voltage-gated channel subfamily Q member 4

potassium voltage-gated channel subfamily KQT member 4

Potassium voltage-gated channel subfamily KQT member 4

KCNQ4_HUMAN

The protein encoded by this gene forms a potassium channel that is thought to play a critical role in the regulation of neuronal excitability, particularly in sensory cells of the cochlea. The current generated by this channel is inhibited by M1 muscarinic acetylcholine receptors and activated by retigabine, a novel anti-convulsant drug. The encoded protein can form a homomultimeric potassium channel or possibly a heteromultimeric channel in association with the protein encoded by the KCNQ3 gene. Defects in this gene are a cause of nonsyndromic sensorineural deafness type 2 (DFNA2), an autosomal dominant form of progressive hearing loss. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]

KCNQ4: Probably important in the regulation of neuronal excitability. May underlie a potassium current involved in regulating the excitability of sensory cells of the cochlea. KCNQ4 channels are blocked by linopirdin, XE991 and bepridil, whereas clofilium is without significant effect. Muscarinic agonist oxotremorine-M strongly suppress KCNQ4 current in CHO cells in which cloned KCNQ4 channels were coexpressed with M1 muscarinnic receptors. Defects in KCNQ4 are the cause of deafness autosomal dominant type 2A (DFNA2A). DFNA2A is a form of sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. Belongs to the potassium channel family. KQT (TC 1.A.1.15) subfamily. Kv7.4/KCNQ4 sub-subfamily. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, multi-pass; Membrane protein, integral

Chromosomal Location of Human Ortholog: 1p34

Cellular Component: voltage-gated potassium channel complex; integral to membrane; basal plasma membrane; plasma membrane

Molecular Function: potassium channel activity; delayed rectifier potassium channel activity

Biological Process: synaptic transmission; inner ear morphogenesis; sensory perception of sound; potassium ion transport

Disease: Deafness, Autosomal Dominant 2a

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