Rb Anti-NaV1.5

Species Reactivity	Key Applications	Host	Format	Antibody Type
R	WB	Rb	Affinity Purified	Polyclonal Antibody

Species Reactivity

Key Applications

Host

Format

Antibody Type

Affinity Purified

Polyclonal Antibody

Description
Catalogue Number	AB5493-50UL
Brand Family	Chemicon®
Trade Name	Chemicon
Description	Anti-Sodium Channel Nav1.5 Antibody, pain
Alternate Names	SCN5A

Description

Catalogue Number

AB5493-50UL

Brand Family

Chemicon®

Trade Name

Chemicon

Description

Anti-Sodium Channel Nav1.5 Antibody, pain

Alternate Names

SCN5A

Product Information
Format	Affinity Purified
Control	Included free of charge with the antibody is 40 μg of control antigen (lyophilized powder). For negative control, preincubate 1 μg of purified peptide with 1 μg of antibody for one hour at room temperature. Optimal concentrations must be determined by the end user.
Presentation	Affinity purified immunoglobulin. Lyophilized from PBS, pH 7.4, containing 1% BSA, and 0.05% sodium azide. Reconstitute with 50 μL of sterile distilled water. Centrifuge antibody preparation before use (10,000 x g for 5 min).

Product Information

Format

Affinity Purified

Control

Included free of charge with the antibody is 40 μg of control antigen (lyophilized powder). For negative control, preincubate 1 μg of purified peptide with 1 μg of antibody for one hour at room temperature. Optimal concentrations must be determined by the end user.

Presentation

Affinity purified immunoglobulin. Lyophilized from PBS, pH 7.4, containing 1% BSA, and 0.05% sodium azide. Reconstitute with 50 μL of sterile distilled water. Centrifuge antibody preparation before use (10,000 x g for 5 min).

Applications
Application	Anti-Sodium Channel Nav1.5 Antibody, pain is an antibody against Sodium Channel Nav1.5 for use in WB.
Key Applications	Western Blotting
Application Notes	Western blotting: 1:200 using ECL on rat heart membranes. See suggested protocol. Dilutions should be made using a carrier protein such as BSA (1-3%). Optimal working dilutions must be determined by the end user.

Applications

Application

Anti-Sodium Channel Nav1.5 Antibody, pain is an antibody against Sodium Channel Nav1.5 for use in WB.

Key Applications

Western Blotting

Application Notes

Western blotting: 1:200 using ECL on rat heart membranes. See suggested protocol.
Dilutions should be made using a carrier protein such as BSA (1-3%).
Optimal working dilutions must be determined by the end user.

Biological Information
Immunogen	Highly purified peptide corresponding to residues 493-511 of rat Nav1.5 (Accession P15389).
Concentration	Please refer to the Certificate of Analysis for the lot-specific concentration.
Host	Rabbit
Specificity	Recognizes Nav1.5 (Scn5a, SKM2). The epitope specific for Nav1.5 is not present in any other known proteins. SPECIES REACTIVITIES: The immunogen sequence is identical in mouse and conserved in human (17/19). Reactivity with other species has not yet been tested.
Species Reactivity	Rat
Antibody Type	Polyclonal Antibody
Entrez Gene Number	NM_000335.4 NM_001099404.1 NM_001099405.1 NM_198056.2
Entrez Gene Summary	The protein encoded by this gene is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit. This protein is found primarily in cardiac muscle and is responsible for the initial upstroke of the action potential in an electrocardiogram. Defects in this gene are a cause of long QT syndrome type 3 (LQT3), an autosomal dominant cardiac disease. Alternative splicing results in several transcript variants encoding different isoforms.
Gene Symbol	SCN5A HB2 ICCD CMPD2 CMD1E SSS1 HB1 PFHB1 IVF HH1 Nav1.5 CDCD2 HBBD LQT3
UniProt Number	Q14524
UniProt Summary	FUNCTION: SwissProt: Q14524 # This protein 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-resistant Na(+) channel isoform. This channel is responsible for the initial upstroke of the action potential in the electrocardiogram. SIZE: 2016 amino acids; 227162 Da SUBUNIT: Interacts with the PDZ domain of the syntrophin SNTA1, SNTB1 and SNTB2 (By similarity). Interacts with NEDD4, NEDD4L and WWP2. SUBCELLULAR LOCATION: Membrane; Multi-pass membrane protein. TISSUE SPECIFICITY: Expressed in human atrial and ventricular cardiac muscle but not in adult skeletal muscle, brain, myometrium, liver, or spleen. DOMAIN: SwissProt: Q14524 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. PTM: Ubiquitinated by NEDD4L; which promotes its endocytosis. Does not seem to be ubiquitinated by NEDD4 or WWP2. DISEASE: SwissProt: Q14524 # Defects in SCN5A are a cause of progressive familial heart block type I (PFHBI) [MIM:113900]; also known as Lenegre-Lev disease or progressive cardiac conduction defect (PCCD). PFHBI is characterized by progressive alteration of cardiac conduction through the His-Purkinje system with right or left bundle branch block and widening of QRS complexes, leading to complete atrio- ventricular block and causing syncope and sudden death. PFHBI inheritance is autosomal dominant. & Defects in SCN5A are the cause of long QT syndrome type 3 (LQT3) [MIM:603830]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. LQT3 inheritance is an autosomal dominant. & Defects in SCN5A are the cause of Brugada syndrome [MIM:601144]. Brugada syndrome is an autosomal dominant inherited arrhythmia that causes the ventricles to beat so fast that they can prevent the blood from circulating efficiently in the body. When this situation occurs (called ventricular fibrillation), the individual will faint and may die in a few minutes if the heart is not reset. Brugada syndrome is an idiopathic ventricular fibrillation (IVF) syndrome characterized by right bundle branch block and ST elevation on an electrocardiogram (ECG). While Brugada syndrome is a disease that usually affects people in their 30's, it has actually been described at all ages. & Defects in SCN5A are the cause of autosomal recessive sick sinus syndrome 1 (SSS1) [MIM:608567]. The term 'sick sinus syndrome' encompasses a variety of conditions caused by sinus node dysfunction. The most common clinical manifestations are syncope, presyncope, dizziness, and fatigue. Electrocardiogram typically shows sinus bradycardia, sinus arrest, and/or sinoatrial block. Episodes of atrial tachycardias coexisting with sinus bradycardia ('tachycardia-bradycardia syndrome') are also common in this disorder. SSS occurs most often in the elderly associated with underlying heart disease or previous cardiac surgery, but can also occur in the fetus, infant, or child without heart disease or other contributing factors, in which case it is considered to be a congenital disorder. & Defects in SCN5A are a cause of idiopathic ventricular fibrillation (IVF) [MIM:603829]; also called paroxysmal familial ventricular fibrillation. IVF is a self originated, of unknown causation, ventricular fibrillation that causes the ventricles to beat so fast that they can prevent the blood from circulating efficiently in the body. This disorder is not truly idiopathic in many cases but can be caused by specific mutations such as those in the SCN5A gene. IVF is said to cause more than 300,000 sudden deaths each year in the United States alone. In approximately 5 to 12% of cases, there are no demonstrable cardiac or non-cardiac causes to account for the episode, which is therefore classified as idiopathic ventricular fibrillation. & Defects in SCN5A are a cause of sudden infant death syndrome (SIDS) [MIM:272120]. SIDS remains elusive in its causes and devastating in its consequences. Despite the impressive decline in the incidence of SIDS since the recommendation to avoid the prone sleep position, SIDS remains a leading cause of death in the first year of life. & Defects in SCN5A may be a cause of familial atrial standstill [MIM:108770]. Atrial standstill is an extremely rare arrhythmia, characterized by the absence of electrical and mechanical activity in the atria. Electrocardiographically, it is characterized by bradycardia, the absence of P waves, and a junctional narrow complex escape rhythm. & Defects in SCN5A are the cause of dilated cardiomyopathy 1E (CMD1E) [MIM:601154]; also known as dilated cardiomyopathy with conduction disorder and arrhythmia or dilated cardiomyopathy with conduction defect 2. CMD1E is characterized by autosomal dominant transmission, young age of onset, arrhythmia and conduction disorder that culminates, in most cases, in biatrial and biventricular dilation. SIMILARITY: Belongs to the sodium channel family. & Contains 1 IQ domain. MISCELLANEOUS: Na(+) channels in mammalian cardiac membrane have functional properties quite distinct from Na(+) channels in nerve and skeletal muscle.

Biological Information

Immunogen

Highly purified peptide corresponding to residues 493-511 of rat Nav1.5 (Accession P15389).

Concentration

Please refer to the Certificate of Analysis for the lot-specific concentration.

Host

Rabbit

Specificity

Recognizes Nav1.5 (Scn5a, SKM2). The epitope specific for Nav1.5 is not present in any other known proteins.

SPECIES REACTIVITIES:
The immunogen sequence is identical in mouse and conserved in human (17/19). Reactivity with other species has not yet been tested.

Species Reactivity

Antibody Type

Polyclonal Antibody

Entrez Gene Number

Entrez Gene Summary

The protein encoded by this gene is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit. This protein is found primarily in cardiac muscle and is responsible for the initial upstroke of the action potential in an electrocardiogram. Defects in this gene are a cause of long QT syndrome type 3 (LQT3), an autosomal dominant cardiac disease. Alternative splicing results in several transcript variants encoding different isoforms.

Gene Symbol

SCN5A
HB2
ICCD
CMPD2
CMD1E
SSS1
HB1
PFHB1
IVF
HH1
Nav1.5
CDCD2
HBBD
LQT3

UniProt Number

Q14524

UniProt Summary

FUNCTION: SwissProt: Q14524 # This protein 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-resistant Na(+) channel isoform. This channel is responsible for the initial upstroke of the action potential in the electrocardiogram.
SIZE: 2016 amino acids; 227162 Da
SUBUNIT: Interacts with the PDZ domain of the syntrophin SNTA1, SNTB1 and SNTB2 (By similarity). Interacts with NEDD4, NEDD4L and WWP2.
SUBCELLULAR LOCATION: Membrane; Multi-pass membrane protein.
TISSUE SPECIFICITY: Expressed in human atrial and ventricular cardiac muscle but not in adult skeletal muscle, brain, myometrium, liver, or spleen.
DOMAIN: SwissProt: Q14524 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.
PTM: Ubiquitinated by NEDD4L; which promotes its endocytosis. Does not seem to be ubiquitinated by NEDD4 or WWP2.
DISEASE: SwissProt: Q14524 # Defects in SCN5A are a cause of progressive familial heart block type I (PFHBI) [MIM:113900]; also known as Lenegre-Lev disease or progressive cardiac conduction defect (PCCD). PFHBI is characterized by progressive alteration of cardiac conduction through the His-Purkinje system with right or left bundle branch block and widening of QRS complexes, leading to complete atrio- ventricular block and causing syncope and sudden death. PFHBI inheritance is autosomal dominant. & Defects in SCN5A are the cause of long QT syndrome type 3 (LQT3) [MIM:603830]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. LQT3 inheritance is an autosomal dominant. & Defects in SCN5A are the cause of Brugada syndrome [MIM:601144]. Brugada syndrome is an autosomal dominant inherited arrhythmia that causes the ventricles to beat so fast that they can prevent the blood from circulating efficiently in the body. When this situation occurs (called ventricular fibrillation), the individual will faint and may die in a few minutes if the heart is not reset. Brugada syndrome is an idiopathic ventricular fibrillation (IVF) syndrome characterized by right bundle branch block and ST elevation on an electrocardiogram (ECG). While Brugada syndrome is a disease that usually affects people in their 30's, it has actually been described at all ages. & Defects in SCN5A are the cause of autosomal recessive sick sinus syndrome 1 (SSS1) [MIM:608567]. The term 'sick sinus syndrome' encompasses a variety of conditions caused by sinus node dysfunction. The most common clinical manifestations are syncope, presyncope, dizziness, and fatigue. Electrocardiogram typically shows sinus bradycardia, sinus arrest, and/or sinoatrial block. Episodes of atrial tachycardias coexisting with sinus bradycardia ('tachycardia-bradycardia syndrome') are also common in this disorder. SSS occurs most often in the elderly associated with underlying heart disease or previous cardiac surgery, but can also occur in the fetus, infant, or child without heart disease or other contributing factors, in which case it is considered to be a congenital disorder. & Defects in SCN5A are a cause of idiopathic ventricular fibrillation (IVF) [MIM:603829]; also called paroxysmal familial ventricular fibrillation. IVF is a self originated, of unknown causation, ventricular fibrillation that causes the ventricles to beat so fast that they can prevent the blood from circulating efficiently in the body. This disorder is not truly idiopathic in many cases but can be caused by specific mutations such as those in the SCN5A gene. IVF is said to cause more than 300,000 sudden deaths each year in the United States alone. In approximately 5 to 12% of cases, there are no demonstrable cardiac or non-cardiac causes to account for the episode, which is therefore classified as idiopathic ventricular fibrillation. & Defects in SCN5A are a cause of sudden infant death syndrome (SIDS) [MIM:272120]. SIDS remains elusive in its causes and devastating in its consequences. Despite the impressive decline in the incidence of SIDS since the recommendation to avoid the prone sleep position, SIDS remains a leading cause of death in the first year of life. & Defects in SCN5A may be a cause of familial atrial standstill [MIM:108770]. Atrial standstill is an extremely rare arrhythmia, characterized by the absence of electrical and mechanical activity in the atria. Electrocardiographically, it is characterized by bradycardia, the absence of P waves, and a junctional narrow complex escape rhythm. & Defects in SCN5A are the cause of dilated cardiomyopathy 1E (CMD1E) [MIM:601154]; also known as dilated cardiomyopathy with conduction disorder and arrhythmia or dilated cardiomyopathy with conduction defect 2. CMD1E is characterized by autosomal dominant transmission, young age of onset, arrhythmia and conduction disorder that culminates, in most cases, in biatrial and biventricular dilation.
SIMILARITY: Belongs to the sodium channel family. & Contains 1 IQ domain.
MISCELLANEOUS: Na(+) channels in mammalian cardiac membrane have functional properties quite distinct from Na(+) channels in nerve and skeletal muscle.

Product Usage Statements
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.

Product Usage Statements

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 Conditions	Maintain lyophilized material at -20°C for up to 6 months from date of receipt. After reconstitution maintain at -20°C in undiluted aliquots for up to 6 months. Avoid repeated freeze/thaw cycles.

Storage and Shipping Information

Storage Conditions

Maintain lyophilized material at -20°C for up to 6 months from date of receipt. After reconstitution maintain at -20°C in undiluted aliquots for up to 6 months. Avoid repeated freeze/thaw cycles.

Packaging Information
Material Size	50 µL

Packaging Information

Material Size

50 µL

实验耗材

分子生物学试剂

蛋白与免疫学

生化试剂

细胞及检测试剂

色谱及层析

仪器设备

实验服务

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