Sodium Channel Protein Type 9 Subunit Alpha (SCN9A), ELISA Kit

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

Store all reagents at 2-8 degree C

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Small volumes of SCN9A elisa kit 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.

MBS9344311 is a ready-to-use microwell, strip-or-full plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Sodium Channel Protein Type 9 Subunit Alpha (SCN9A) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing SCN9A. The ELISA analytical biochemical technique of the MBS9344311 kit is based on SCN9A antibody-SCN9A antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect SCN9A antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, SCN9A. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

225,214 Da

sodium voltage-gated channel alpha subunit 9

sodium channel protein type 9 subunit alpha

Sodium channel protein type 9 subunit alpha

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SCN9A_HUMAN

This gene encodes a voltage-gated sodium channel which plays a significant role in nociception signaling. Mutations in this gene have been associated with primary erythermalgia, channelopathy-associated insensitivity to pain, and paroxysmal extreme pain disorder. [provided by RefSeq, Aug 2009]

SCN9A: Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-sensitive Na(+) channel isoform. Plays a role in pain mechanisms, especially in the development of inflammatory pain. Defects in SCN9A are the cause of primary erythermalgia (PERYTHM). It is an autosomal dominant disease characterized by recurrent episodes of severe pain associated with redness and warmth in the feet or hands. Defects in SCN9A are the cause of congenital indifference to pain autosomal recessive (CIPAR); also known as channelopathy-associated insensitivity to pain. A disorder characterized by congenital inability to perceive any form of pain, in any part of the body. All other sensory modalities are preserved and the peripheral and central nervous systems are apparently intact. Patients perceive the sensations of touch, warm and cold temperature, proprioception, tickle and pressure, but not painful stimuli. There is no evidence of a motor or sensory neuropathy, either axonal or demyelinating. Defects in SCN9A are a cause of paroxysmal extreme pain disorder (PEPD); previously known as familial rectal pain (FRP). PEPD is an autosomal dominant paroxysmal disorder of pain and autonomic dysfunction. The distinctive features are paroxysmal episodes of burning pain in the rectal, ocular, and mandibular areas accompanied by autonomic manifestations such as skin flushing. Defects in SCN9A are a cause of generalized epilepsy with febrile seizures plus type 7 (GEFS+7). GEFS+7 is a rare autosomal dominant, familial condition with incomplete penetrance and large intrafamilial variability. Patients display febrile seizures persisting sometimes beyond the age of 6 years and/or a variety of afebrile seizure types. This disease combines febrile seizures, generalized seizures often precipitated by fever at age 6 years or more, and partial seizures, with a variable degree of severity. Defects in SCN9A are the cause of familial febrile convulsions type 3B (FEB3B). FEB3B consists of seizures associated with febrile episodes in childhood without any evidence of intracranial infection or defined pathologic or traumatic cause. It is a common condition, affecting 2-5% of children aged 3 months to 5 years. The majority are simple febrile seizures (generally defined as generalized onset, single seizures with a duration of less than 30 minutes). Complex febrile seizures are characterized by focal onset, duration greater than 30 minutes, and/or more than one seizure in a 24 hour period. The likelihood of developing epilepsy following simple febrile seizures is low. Complex febrile seizures are associated with a moderately increased incidence of epilepsy. Belongs to the sodium channel (TC 1.A.1.10) family. Nav1.7/SCN9A subfamily. 3 isoforms of the human protein are produced by alternative splicing.

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

Chromosomal Location of Human Ortholog: 2q24

Cellular Component: plasma membrane; voltage-gated sodium channel complex

Molecular Function: sodium ion binding; voltage-gated sodium channel activity

Biological Process: behavioral response to pain; generation of action potential; inflammatory response; post-embryonic development; response to toxin; sodium ion transport

Disease: Epileptic Encephalopathy, Early Infantile, 6; Erythermalgia, Primary; Generalized Epilepsy With Febrile Seizures Plus, Type 7; Indifference To Pain, Congenital, Autosomal Recessive; Neuropathy, Hereditary Sensory And Autonomic, Type Iia; Paroxysmal Extreme Pain Disorder

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