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產品訂購信息：
英文名稱  Anti-Nav1.5/SCN5A 

中文名稱   電壓門控鈉通道5α抗體品牌 

別    名  Cardiac tetrodotoxin insensitive voltage dependent sodium channel alpha subunit; CDCD2; CMD1E; CMPD2; HB1; HB2; HBBD; HH1; ICCD; IVF; LQT3; PFHB1; Scn5a (gene name); Scn5a; SCN5A_HUMAN; Sodium channel protein cardiac muscle alpha subunit; Sodium channel protein cardiac muscle alpha-subunit; Sodium channel protein cardiac muscle subunit alpha; Sodium channel protein type 5 subunit alpha; Sodium channel protein type V alpha subunit; Sodium channel protein type V subunit alpha; SSS1; VF1; Voltage gated sodium channel alpha subunit Nav1.5; Voltage-gated sodium channel alpha subunit Nav1.5; Voltage-gated sodium channel subunit alpha Nav1.5.

濃    度   1mg/1ml

規(guī) 格  0.2ml/200μg

抗體來源   Rabbit

克隆類型   polyclonal

交叉反應   Human, Mouse, Rat, Chicken, Dog, Pig, Horse, Rabbit, Zebrafish, Sheep, Chimpanzee, mpanzee 

產品類型   一抗  

研究領域    

蛋白分子量  predicted molecular weight: 227kDa

性    狀   Lyophilized or Liquid

免 疫 原 KLH conjugated synthetic peptide derived from human Nav1.5/SCN5A 

亞    型   IgG

純化方法   affinity purified by Protein A

儲 存 液   Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4

電壓門控鈉通道5α抗體品牌 產品應用    ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:50-200

（石蠟切片需做抗原修復） 

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

保存條件  Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. 

Important Note  This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 

產品介紹 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.

Function : 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. Channel inactivation is regulated by intracellular calcium levels.

Subunit : Interacts with the PDZ domain of the syntrophin SNTA1, SNTB1 and SNTB2 (By similarity). Interacts with NEDD4, NEDD4L, WWP2 and GPD1L. Interacts with CALM. Interacts with FGF13; the interaction is direct and may regulate SNC5A density at membranes and function.

Subcellular Location : Membrane.

Tissue Specificity : Found in jejunal circular smooth muscle cells (at protein level). Expressed in human atrial and ventricular cardiac muscle but not in adult skeletal muscle, brain, myometrium, liver, or spleen. Isoform 4 is expressed in brain.

Post-translational modifications : Regulated through phosphorylation by CaMK2D (By similarity).

Ubiquitinated by NEDD4L; which promotes its endocytosis. Does not seem to be ubiquitinated by NEDD4 or WWP2.

DISEASE : Defects in SCN5A are a cause of progressive familial heart block type 1A (PFHB1A) [MIM:113900]; also known as Lenegre-Lev disease or progressive cardiac conduction defect (PCCD). PFHB1A is an autosomal dominant cardiac bundle branch disorder that may progress to complete heart block. PFHB1A 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 atrioventricular block and causing syncope and sudden death. [DISEASE] 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 type 1 (BRGDA1) [MIM:601144]. An autosomal dominant tachyarrhythmia characterized by right bundle branch block and ST segment elevation on an electrocardiogram (ECG). It can cause the ventricles to beat so fast that the blood is prevented 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.

Defects in SCN5A are the cause of sick sinus syndrome type 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 the cause of familial paroxysmal ventricular fibrillation type 1 (VF1) [MIM:603829]. A cardiac arrhythmia marked by fibrillary contractions of the ventricular muscle due to rapid repetitive excitation of myocardial fibers without coordinated contraction of the ventricle and by absence of atrial activity.

Defects in SCN5A may be a cause of sudden infant death syndrome (SIDS) [MIM:272120]. SIDS is the sudden death of an infant younger than 1 year that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of clinical history. Pathophysiologic mechanisms for SIDS may include respiratory dysfunction, cardiac dysrhythmias, cardiorespiratory instability, and inborn errors of metabolism, but definitive pathogenic mechanisms precipitating an infant sudden death remain elusive. Long QT syndromes-associated mutations can be responsible for some of SIDS cases.

Defects in SCN5A may be a cause of familial atrial standstill (FAS) [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 cardiomyopathy dilated type 1E (CMD1E) [MIM:601154]; also known as dilated cardiomyopathy with conduction disorder and arrhythmia or dilated cardiomyopathy with conduction defect 2. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.

Defects in SCN5A are the cause of familial atrial fibrillation type 10 (ATFB10) [MIM:614022]. ATFB10 is a familial form of atrial fibrillation, a common sustained cardiac rhythm disturbance. Atrial fibrillation is characterized by disorganized atrial electrical activity and ineffective atrial contraction promoting blood stasis in the atria and reduces ventricular filling. It can result in palpitations, syncope, thromboembolic stroke, and congestive heart failure.

Similarity : Belongs to the sodium channel (TC 1.A.1.10) family. Nav1.5/SCN5A subfamily.

Contains 1 IQ domain.

Database links : UniProtKB/Swiss-Prot: Q14524.2

Involvement in disease;Defects in SCN5A are a cause of progressive familial heart block type 1A (PFHB1A); also known as Lenegre-Lev disease or progressive cardiac conduction defect (PCCD). PFHB1A is an autosomal dominant cardiac bundle branch disorder that may progress to complete heart block. PFHB1A 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.

Defects in SCN5A are the cause of long QT syndrome type 3 (LQT3). 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 type 1 (BRS1). BRS1 is an autosomal dominant tachyarrhythmia characterized by right bundle branch block and ST segment elevation on an electrocardiogram (ECG). It can cause the ventricles to beat so fast that the blood is prevented 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.

改良麥康凱肉湯凍干配套試劑SR0240支添加于(025(025

Peptone 140 (Soytone) 蛋白胨-140 100g incubation media Peptone 140 (Soytone) 蛋白胨-140 100g

小腸耶爾森氏菌 酒精酵母 支/瓶

大腸桿菌顯色培養(yǎng)基l用于快速、準確檢測大腸桿菌，培養(yǎng)24小時，顯藍綠色

MiddleBrook7H10瓊脂 250g 用于分枝桿菌的分離培養(yǎng)

改良沙氏瓊脂培養(yǎng)基250g用于真菌培養(yǎng)

LB瓊脂 250(g) incubation media LB瓊脂 250(g)

NZM肉湯 NZM Broth 100克 BR

KF鏈球菌瓊脂于鏈球菌的選擇性分離及計數(SN標準)incubationmediaKF鏈球菌瓊脂于鏈球菌的選擇性分離及計數(SN標準)

霍亂紅胨水 20支 霍亂弧菌的霍亂紅試驗

月桂基鹽胰蛋白胨肉湯(LST)2220g用于多管發(fā)酵法測定大腸菌群和糞大腸菌GB4789.3-20/T4789.38-2008，GB/T4789.39-200...

MRVP 培養(yǎng)基 (Clarks and Lubs 培養(yǎng)基) (CM0043) Oxoid incubation media MRVP 培養(yǎng)基 (Clarks and Lubs 培養(yǎng)基) (CM0043) Oxoid

耐久腸球菌(堅韌鏈球菌) 支/瓶

SD-39Agar

MycoplasmaSemi-fluidMedium

CL-0164NAMALWA(人Butt's細胞)5×106cells/瓶×2

CD84 Others Cynomolgus 食蟹猴 CD84 人細胞裂解液 (陽性對照)

人成纖維細胞-心室裂解物HCF-av L

CCD-1095Sk細胞，人浸潤性導管癌旁皮膚細胞 鼠細胞,H22-H8D8細胞 腦成纖維細胞Many types of cells包裝：5 × 105次方(1ml)

BC3H1(小鼠細胞) 5×106cells/瓶×2

HUASMC Pellet 人臍動脈平滑肌細胞團塊 > 1 mio.cells 人上皮細胞裂解物HPEpiCL

電壓門控鈉通道5α抗體品牌CL-0162MS1(小鼠胰島內皮細胞)5×106cells/瓶×2

F7 Others Mouse 小鼠 Coagulation Factor VII / FVII / F7 CHO細胞裂解液 (陽性對照)

人心肌細胞-裂解物HCM-a L

家豬皮膚細胞;SSC-S1 癌細胞，ZR-75-1細胞 NS1細胞，小鼠細胞

腺病毒轉化的人胚腎細胞;AAV-293

HA Others H5N1 甲型 H5N1 (A/chicken/Egypt/2253-1/2006) 血凝素HA1 (Hemagglutinin) 人細胞裂解液 (陽性對照)

抗體的生物素化標記實驗要點：

1. 電壓門控鈉通道5α抗體品牌 如在反應混合液中有疊氮鈉或游離氨基存在,會抑制標記反應。因此,蛋白質在反應前要對 0.1mol/L碳酸氫鈉緩沖液或0.5mol/L硼酸緩沖液充分透析；

2.所用的NHSB及待生物素化蛋白質之間的分子比按蛋白質表面的ε-氨基的密度會有所不同,選擇不當則影響標記的效率,應先用幾個不同的分子比來篩選最適條件；

3.用NHSB量過量也是不利的,抗原的結合位點可能因此被封閉,導致抗體失活；

4.由于抗體的氨基不易接近可能造成生物素化不足,此時可加入去污劑如 Triton x-100, Tween20等；

5.當游離ε-氨基(賴氨酸殘基的氨基)存在于抗體的抗原結合位點時,或位于酶的催化位點時,生物素化會降低或損傷抗體蛋白的結合力或活性；

6.生物素還可能與不同的功能基團,如羰基、氨基、巰基、異咪唑基及苯酚基,也可與糖基共價結合；

7.交聯反應后,應充分透析,否則,殘余的生物素會對生物素化抗體與親和素的結合產生競爭作用；

8.在細胞的熒光標記實驗中,中和親和素的本底低,但由于鏈霉親和素含有少量正電荷,故對某些細胞可導致高本底。

抗體的鑒定：

1）電壓門控鈉通道5α抗體品牌 抗體的效價鑒定：不管是用于診斷還是用于,制備抗體的目的都是要求較高效價。不同的抗原制備的抗體,要求的效價不一。鑒定效價的方法很多,包括有試管凝集反應,瓊脂擴散試驗,酶聯免疫吸附試驗等。常用的抗原所制備的抗體一般都有約成的鑒定效價的方法,以資比較。如制備抗抗體的效價,一般就采用瓊脂擴散試驗來鑒定。

2）抗體的特異性鑒定：抗體的特異性是指與相應抗原或近似抗原物質的識別能力。抗體的特異性高,它的識別能力就強。衡量特異性通常以交叉反應率來表示。交叉反應率可用競爭抑制試驗測定。以不同濃度抗原和近似抗原分別做競爭抑制曲線,計算各自的結合率,求出各自在IC50時的濃度,并按公式計算交叉反應率。 

如果所用抗原濃度IC50濃度為pg/管,而一些近似抗原物質的IC50濃度幾乎是無窮大時,表示這一抗血清與其他抗原物質的交叉反應率近似為0,即該血清的特異性較好。

3）抗體親和力：是指抗體和抗原結合的牢固程度。親和力的高低是由抗原分子的大小,抗體分子的結合位點與抗原決定簇之間立體構型的合適度決定的。有助于維持抗原抗體復合物穩(wěn)定的分子間力有氫鍵,疏水鍵,側鏈相反電荷基因的庫侖力,范德華力和空間斥力。親和力常以親和常數K表示,K的單位是L/mol。抗體親和力的測定對抗體的篩選,確定抗體的用途,驗證抗體的均一性等均有重要意義。