06-811 | Anti-Na+ Channel α Antibody, cardiac (III-IV loop)

06-811
200 µg  
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      Overview

      Replacement Information

      Key Spec Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      VrtICC, IP, WBRbPurifiedPolyclonal Antibody
      Description
      Catalogue Number06-811
      Brand Family Upstate
      Trade Name
      • Upstate
      DescriptionAnti-Na+ Channel α Antibody, cardiac (III-IV loop)
      Background InformationVoltage-gated sodium channels in the brain are characterized into three subtypes: brain type I, type II and type III based on function and structure. Antibodies against these subtypes consist of a principle alpha subunit with variable isoforms and two auxiliary subunits termed β1 and β2.
      References
      Product Information
      FormatPurified
      Control
      • Tested on rat brain microsomal lysate
      PresentationPurified in PBS with 0.05% NaN3 and 30% Glycerol
      Applications
      ApplicationThis Anti-Na+ Channel α Antibody, cardiac (III-IV loop) is validated for use in IC, IP, WB for the detection of Na+ Channel α.
      Key Applications
      • Immunocytochemistry
      • Immunoprecipitation
      • Western Blotting
      Application NotesWestern Blot: 0.5-2 μg/mL of this lot detected Na+ Channel (III-IV loop) in 20 μg Rat Brain Microsomal Prep. (Catalog # 12-144).

      Immunoprecipitation:
      1-4 μg of a previous lot immunoprecipitated Na+ Channel (III-IV loop) from 400 μg of Rat Brain Microsomal Prep.

      Immunocytochemistry:
      (See photo1) Mouse sciatic nerves stained with cat. # 06-811 at 20 µg/mL.
      Biological Information
      HostRabbit
      Specificitysodium channel intracellular III-IV loop
      IsotypeIgG
      Species Reactivity
      • Vertebrates
      Antibody TypePolyclonal Antibody
      Entrez Gene Number
      Entrez Gene SummaryThe vertebrate sodium channel is a voltage-gated ion channel essential for the generation and propagation of action potentials, chiefly in nerve and muscle. Voltage-sensitive sodium channels are heteromeric complexes consisting of a large central pore-forming glycosylated alpha subunit and 2 smaller auxiliary beta subunits. Functional studies have indicated that the transmembrane alpha subunit of the brain sodium channels is sufficient for expression of functional sodium channels (Goldin et al., 1986 [PubMed 2429308]; Isom, 2002 [PubMed 11779698]).[supplied by OMIM]
      Gene Symbol
      • SCN1A
      • HBSCI
      • Nav1.1
      • FEB3
      • NAC1
      • GEFSP2
      • SCN1
      • SMEI
      Purification MethodProtein A chromatography
      UniProt Number
      UniProt SummaryFUNCTION: SwissProt: P35498 # 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.
      SIZE: 2009 amino acids; 228972 Da
      SUBUNIT: The sodium channel consists of a large polypeptide and 2- 3 smaller ones. This sequence represents a large polypeptide.
      SUBCELLULAR LOCATION: Membrane; Multi-pass membrane protein.
      DOMAIN: SwissProt: P35498 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.
      DISEASE: SwissProt: P35498 # Defects in SCN1A are the cause of generalized epilepsy with febrile seizures plus type 2 (GEFS+2) [MIM:604233]. This autosomal dominant disorder is characterized by febrile seizures in children and afebrile seizures in adults. Penetrance is incomplete and a large intrafamilial variability of the phenotype is observed. & Defects in SCN1A are a cause of severe myoclonic epilepsy in infancy (SMEI) [MIM:607208]; also called Dravet syndrome. SMEI is a severe form of generalized epilepsy with febrile seizures. It is a rare disorder characterized by normal development before onset, seizures beginning in the first year of life in the form of generalized or unilateral febrile clonic seizures, secondary appearance of myoclonic seizures, and occasionally partial seizures. It is associated with ataxia, slowed psychomotor development, and mental decline. & Defects in SCN1A are the cause of familial hemiplegic migraine 3 (FHM3) [MIM:609634]. FHM3 is an autosomal dominant severe subtype of migraine with aura characterized by some degree of hemiparesis during the attacks. The episodes are associated with variable features of nausea, vomiting, photophobia and phonophobia. Age at onset ranges from 6 to 15 years. Some patients may manifest seizures during infancy. & Defects in SCN1A are the cause of familial febrile convulsions 3 (FEB3) [MIM:604403]; also known as familial febrile seizures 3. Febrile convulsions affect 5-12% of infants and children up to 6 years of age. There is epidemiological evidence that febrile seizures are associated with subsequent afebrile and unprovoked seizures in 2% to 7% of patients. Inheritance pattern is autosomal dominant.
      SIMILARITY: Belongs to the sodium channel family. & Contains 1 IQ domain.
      Molecular Weight220 kDa
      Physicochemical Information
      Dimensions
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Quality Assuranceroutinely evaluated by immunoblot on Rat Brain Microsomal Prep
      Usage Statement
      • Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
      Storage and Shipping Information
      Storage ConditionsMaintain at -20°C in undiluted aliquots for up to 1 year after date of receipt.
      Packaging Information
      Material Size200 µg
      Transport Information
      Supplemental Information
      Specifications

      Documentation

      SDS

      Title

      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number
      Anti-Na+ Channel (III-IV loop) - 2135170 2135170
      Anti-Na+ Channel (III-IV loop) - DAM1745306 DAM1745306
      Anti-Na+ Channel (III-IV loop) - DAM1787871 DAM1787871
      Anti-Na+ Channel (III-IV loop) -2544305 2544305
      Anti-Na+ Channel (III-IV loop) -2588494 2588494
      Anti-Na+ Channel (III-IV loop) -2608397 2608397
      Anti-Na+ Channel alpha;, cardiac (III-IV loop) - 16826 16826
      Anti-Na+ Channel alpha;, cardiac (III-IV loop) - 21625 21625
      Anti-Na+ Channel alpha;, cardiac (III-IV loop) - 26413 26413

      References

      Reference overviewApplicationPub Med ID
      Sodium channelopathy induced by mild axonal trauma worsens outcome after a repeat injury.
      Yuen, TJ; Browne, KD; Iwata, A; Smith, DH
      Journal of neuroscience research  87  3620-5  2009

      Show Abstract
      Immunofluorescence19565655 19565655
      Cardiac sulfonylurea receptor short form-based channels confer a glibenclamide-insensitive KATP activity.
      Jie-Lin Pu,Bin Ye,Stacie L Kroboth,Elizabeth M McNally,Jonathan C Makielski,Nian-Qing Shi
      Journal of molecular and cellular cardiology  44  2008

      Show Abstract Full Text Article
      18001767 18001767
      Traumatic axonal injury induces proteolytic cleavage of the voltage-gated sodium channels modulated by tetrodotoxin and protease inhibitors.
      Iwata, A; Stys, PK; Wolf, JA; Chen, XH; Taylor, AG; Meaney, DF; Smith, DH
      The Journal of neuroscience : the official journal of the Society for Neuroscience  24  4605-13  2004

      Show Abstract
      15140932 15140932
      Potassium channel distribution, clustering, and function in remyelinating rat axons
      Rasband, M. N., et al
      J Neurosci, 18:36-47 (1998)  1998

      Immunofluorescence9412484 9412484
      The clustering of axonal sodium channels during development of the peripheral nervous system
      Vabnick, I., et al
      J Neurosci, 16:4914-22 (1996)  1996

      Immunocytochemistry8756423 8756423
      Immunocytochemical investigations of sodium channels along nodal and internodal portions of demyelinated axons
      England, J. D., et al
      Microsc Res Tech, 34:445-51 (1996)  1996

      Immunocytochemistry8837020 8837020
      Clustering of Na+ channels and node of Ranvier formation in remyelinating axons
      Dugandzija-Novakovic, S., et al
      J Neurosci, 15:492-503 (1995)  1995

      Immunocytochemistry7823157 7823157
      Increased numbers of sodium channels form along demyelinated axons.
      England, J D, et al.
      Brain Res., 548: 334-7 (1991)  1991

      Show Abstract
      1651145 1651145
      Principal glycopeptide of the tetrodotoxin/saxitoxin binding protein from Electrophorus electricus: isolation and partial chemical and physical characterization.
      Miller, J A, et al.
      Biochemistry, 22: 462-70 (1983)  1983

      Show Abstract
      6186277 6186277

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      Categories

      Life Science Research > Antibodies and Assays > Primary Antibodies