ELISA/assay

Monkey Nav1.7 ELISA Kit

MBS745666

48-Strip-Wells

470 USD

ELISA Kit

Monkey Nav1.7 ELISA Kit

Nav1.7

Nav1.7, partial; Sodium channel protein type 9 subunit alpha; Neuroendocrine sodium channel; hNE-Na; Peripheral sodium channel 1; PN1; Sodium channel protein type IX subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.7

Nav1.7

SCN9A; NENA; hNE-Na; PN1

SCN9A_HUMAN

Monkey

This assay has high sensitivity and excellent specificity for detection of Nav1.7. No significant cross-reactivity or interference between Nav1.7 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between Nav1.7 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 0.1 ng/mL.

Intended Uses: This Nav1.7 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Monkey Nav1.7. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Principle of the assay: Nav1.7 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-Nav1.7 antibody and an Nav1.7-HRP conjugate. The assay sample and buffer are incubated together with Nav1.7-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the Nav1.7 concentration since Nav1.7 from samples and Nav1.7-HRP conjugate compete for the anti-Nav1.7 antibody binding site. Since the number of sites is limited, as more sites are occupied by Nav1.7 from the sample, fewer sites are left to bind Nav1.7-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The Nav1.7 concentration in each sample is interpolated from this standard curve.

18073671

CAC84551.1

Q15858

225,227 Da

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: Channel, sodium; Membrane protein, integral; Membrane protein, multi-pass. Chromosomal Location of Human Ortholog: 2q24. Cellular Component: voltage-gated sodium channel complex; plasma membrane. Molecular Function: sodium ion binding; voltage-gated sodium channel activity. Biological Process: behavioral response to pain; response to toxin; sodium ion transport; generation of action potential; inflammatory response; post-embryonic development. Disease: Neuropathy, Hereditary Sensory And Autonomic, Type Iia; Generalized Epilepsy With Febrile Seizures Plus, Type 7; Erythermalgia, Primary; Paroxysmal Extreme Pain Disorder; Epileptic Encephalopathy, Early Infantile, 6; Indifference To Pain, Congenital, Autosomal Recessive

48-Strip-Wells

470 USD

96-Strip-Wells

675