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CHRNA10 Antibody (Center)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | Q9GZZ6 |
| Other Accession | Q9JLB5, NP_065135.2 |
| Reactivity | Human |
| Predicted | Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 49705 Da |
| Antigen Region | 179-206 aa |
| Gene ID | 57053 |
|---|---|
| Other Names | Neuronal acetylcholine receptor subunit alpha-10, Nicotinic acetylcholine receptor subunit alpha-10, NACHR alpha-10, CHRNA10, NACHRA10 |
| Target/Specificity | This CHRNA10 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 179-206 amino acids from the Central region of human CHRNA10. |
| Dilution | WB~~1:1000 IHC-P~~1:10~50 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | CHRNA10 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | CHRNA10 (HGNC:13800) |
|---|---|
| Synonyms | NACHRA10 |
| Function | Component of neuronal acetylcholine receptors (nAChRs) that function as pentameric, ligand-gated cation channels with high calcium permeability. nAChRs are excitatory neurotrasnmitter receptors formed by a collection of nAChR subunits. Each nAchR subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, cation permeability, and binding to allosteric modulators (Probable). Forms heteropentamers with CHRNA9. Expressed in the inner ear, in sympathetic neurons and in other non-neuronal cells, such as skin keratinocytes and lymphocytes (PubMed:11752216, PubMed:15531379). nAChR formed by CHRNA9:CHRNA10 is involved in modulation of auditory stimuli. The channel is permeable to a range of divalent cations including calcium, the influx of which may activate a potassium current which hyperpolarizes the cell membrane. In the ear, mediates synaptic transmission between efferent olivocochlear fibers and hair cells of the cochlea, this may lead to a reduction in basilar membrane motion, altering the activity of auditory nerve fibers and reducing the range of dynamic hearing (PubMed:11752216). This may protect against acoustic trauma. May also regulate keratinocyte adhesion (By similarity). |
| Cellular Location | Synaptic cell membrane {ECO:0000250|UniProtKB:Q9JLB5}; Multi-pass membrane protein. Cell membrane {ECO:0000250|UniProtKB:Q9JLB5}; Multi-pass membrane protein |
| Tissue Location | Expressed in inner-ear tissue, tonsil, immortalized B-cells, cultured T-cells and peripheral blood lymphocytes |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
CHRNA10 is an ionotropic receptor with a probable role in the modulation of auditory stimuli. Agonist binding may induce an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. The channel is permeable to a range of divalent cations including calcium, the influx of which may activate a potassium current which hyperpolarizes the cell membrane. In the ear, this may lead to a reduction in basilar membrane motion, altering the activity of auditory nerve fibers and reducing the range of dynamic hearing. This may protect against acoustic trauma.
References
Saccone, N.L., et al. Genes Brain Behav. 9(7):741-750(2010)
Rose, J.E., et al. Mol. Med. 16 (7-8), 247-253 (2010) :
Rigbi, A., et al. Pharmacogenomics J. (2010) In press :
Need, A.C., et al. Eur. J. Hum. Genet. 17(7):946-957(2009)
Saccone, N.L., et al. Am. J. Med. Genet. B Neuropsychiatr. Genet. 150B (4), 453-466 (2009) :
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