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Goat Anti-KCNQ4 Antibody
Peptide-affinity purified goat antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | P56696 |
| Other Accession | NP_751895, 9132 |
| Reactivity | Human |
| Host | Goat |
| Clonality | Polyclonal |
| Concentration | 100ug/200ul |
| Isotype | IgG |
| Calculated MW | 77101 Da |
| Gene ID | 9132 |
|---|---|
| Other Names | Potassium voltage-gated channel subfamily KQT member 4, KQT-like 4, Potassium channel subunit alpha KvLQT4, Voltage-gated potassium channel subunit Kv7.4, KCNQ4 |
| Format | 0.5 mg IgG/ml in Tris saline (20mM Tris pH7.3, 150mM NaCl), 0.02% sodium azide, with 0.5% bovine serum albumin |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Goat Anti-KCNQ4 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | KCNQ4 |
|---|---|
| Function | 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 muscarinic receptors. |
| Cellular Location | Basal cell membrane; Multi-pass membrane protein. Note=Situated at the basal membrane of cochlear outer hair cells |
| Tissue Location | Expressed in the outer, but not the inner, sensory hair cells of the cochlea. Slightly expressed in heart, brain and skeletal muscle |
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
DFNA2 Nonsyndromic Hearing Loss Smith RJH, et al. , 1993. PMID 20301388.
Replication of previous genome-wide association studies of bone mineral density in premenopausal American women. Ichikawa S, et al. J Bone Miner Res, 2010 Aug. PMID 20200978.
Analysis of gene polymorphisms associated with K ion circulation in the inner ear of patients susceptible and resistant to noise-induced hearing loss. Pawelczyk M, et al. Ann Hum Genet, 2009 Jul. PMID 19523148.
Audioprofile-directed screening identifies novel mutations in KCNQ4 causing hearing loss at the DFNA2 locus. Hildebrand MS, et al. Genet Med, 2008 Nov. PMID 18941426.
KCNQ4 mutations associated with nonsyndromic progressive sensorineural hearing loss. Nie L. Curr Opin Otolaryngol Head Neck Surg, 2008 Oct. PMID 18797286.
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