Product datasheet
Anti-Nav1.7 antibody [S68-6] - C-terminal (HRP)
ab183415
Overview
Product name
Anti-Nav1.7 antibody [S68-6] - C-terminal (HRP)
Description
Mouse monoclonal [S68-6] to Nav1.7 - C-terminal (HRP)
Conjugation
HRP
Tested applications
WB, IHC-P, IHC-Fr, ICC/IF
Species reactivity
Reacts with: Mouse, Rat, Human, Chinese Hamster
Predicted to work with: Rabbit
Immunogen
Recombinant fragment aa 1751-1946 (C terminal). NCBI Accession No. NP_002968.1
Sequence:
NFSVATEESTEPLSEDDFEMFYEVWEKFDPDATQFIEFSKLSDFAAALDP
PLLIAKPNKVQLIAMDLPMVSGDRIHCLDILFAFTKRVLGESGEMDSLRS
QMEERFMSANPSKVSYEPITTTLKRKQEDVSATVIQRAYRRYRLRQNVKN
ISSIYIKDGDRDDDLLNKKDMAFDNVNENSSPEKTDATSSTTSPPS
Database link: Q15858
Run BLAST with
Positive control
Run BLAST with
HEK 293 cell lysate transiently expressing Nav1.7. Chinese Hamster CHO cell lysate. Mouse
brain tissue.
Properties
Form
Liquid
Storage instructions
Shipped at 4°C. Store at +4°C.
Storage buffer
pH: 7.4
Preservative: 0.09% Sodium azide
Constituents: 50% Glycerol, 49% PBS
Purity
Protein G purified
Clonality
Monoclonal
Clone number
S68-6
Isotype
IgG1
Applications
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Our Abpromise guarantee covers the use of ab183415 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application
WB
Abreviews
Notes
Use a concentration of 1 - 10 µg/ml.
1 μg/mL of ab183415 was sufficient to detect Nav1.7 in 10 μg of HEK 293 cell
lysate transiently expressing Nav1.7 by colorimetric immunoblot analysis using
Goat anti-mouse IgG:HRP as the secondary antibody
IHC-P
Use a concentration of 0.1 - 1 µg/ml.
IHC-Fr
Use a concentration of 0.1 - 1 µg/ml.
ICC/IF
Use a concentration of 1 - 10 µg/ml.
Target
Function
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.
Tissue specificity
Expressed strongly in dorsal root ganglion, with only minor levels elsewhere in the body, smooth
muscle cells, MTC cell line and C-cell carcinoma. Isoform 1 is expressed preferentially in the
central and peripheral nervous system. Isoform 2 is expressed preferentially in the dorsal root
ganglion.
Involvement in disease
Defects in SCN9A are the cause of primary erythermalgia (PERYTHM) [MIM:133020]. 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) [MIM:243000]; 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) [MIM:167400];
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) [MIM:604233]. 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) [MIM:604403].
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).
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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.
Sequence similarities
Belongs to the sodium channel (TC 1.A.1.10) family. Nav1.7/SCN9A subfamily.
Contains 1 IQ domain.
Domain
The sequence contains 4 internal repeats, each with 5 hydrophobic segments (S1,S2,S3,S5,S6)
and one positively charged segment (S4). Segments S4 are probably the voltage-sensors and
are characterized by a series of positively charged amino acids at every third position.
Post-translational
modifications
Ubiquitinated by NEDD4L; which may promote its endocytosis. Does not seem to be
ubiquitinated by NEDD4.
Cellular localization
Membrane. In neurite terminals.
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