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| 產(chǎn)地 | 進(jìn)口、國(guó)產(chǎn) |
| 品牌 | 上海莼試 |
| 保存條件 | Store at -20 °C |
| 貨號(hào) | CS12371 |
| 應(yīng)用范圍 | ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:50-200 |
| CAS編號(hào) | |
| 抗體名 | Anti-Nav1.5/SCN5A |
| 克隆性 | 是 |
| 靶點(diǎn) | 詳見(jiàn)說(shuō)明書 |
| 適應(yīng)物種 | 詳見(jiàn)說(shuō)明書 |
| 形態(tài) | 詳見(jiàn)說(shuō)明書 |
| 宿主 | 詳見(jiàn)說(shuō)明書 |
| 亞型 | IgG |
| 標(biāo)識(shí)物 | 詳見(jiàn)說(shuō)明書 |
| 濃度 | 1mg/1ml% |
| 免疫原 | KLH conjugated synthetic peptide derived from human Nav1.5/SCN5A |
產(chǎn)品訂購(gòu)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(lái)源 Rabbit
克隆類型 polyclonal
交叉反應(yīng) Human, Mouse, Rat, Chicken, Dog, Pig, Horse, Rabbit, Zebrafish, Sheep, Chimpanzee, mpanzee
產(chǎn)品類型 一抗
研究領(lǐng)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(chǔ) 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(chǎn)品應(yīng)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(fù)）
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(chǎn)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(zhǔn)確檢測(cè)大腸桿菌，培養(yǎng)24小時(shí)，顯藍(lán)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(jì)數(shù)(SN標(biāo)準(zhǔn))incubationmediaKF鏈球菌瓊脂于鏈球菌的選擇性分離及計(jì)數(shù)(SN標(biāo)準(zhǔn))
霍亂紅胨水 20支 霍亂弧菌的霍亂紅試驗(yàn)
月桂基鹽胰蛋白胨肉湯(LST)2220g用于多管發(fā)酵法測(cè)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(jiān)韌鏈球菌) 支/瓶
SD-39Agar
MycoplasmaSemi-fluidMedium
CL-0164NAMALWA(人Butt's細(xì)胞)5×106cells/瓶×2
CD84 Others Cynomolgus 食蟹猴 CD84 人細(xì)胞裂解液 (陽(yáng)性對(duì)照)
人成纖維細(xì)胞-心室裂解物HCF-av L
CCD-1095Sk細(xì)胞，人浸潤(rùn)性導(dǎo)管癌旁皮膚細(xì)胞 鼠細(xì)胞,H22-H8D8細(xì)胞 腦成纖維細(xì)胞Many types of cells包裝：5 × 105次方(1ml)
BC3H1(小鼠細(xì)胞) 5×106cells/瓶×2
HUASMC Pellet 人臍動(dòng)脈平滑肌細(xì)胞團(tuán)塊 > 1 mio.cells 人上皮細(xì)胞裂解物HPEpiCL
電壓門控鈉通道5α抗體品牌CL-0162MS1(小鼠胰島內(nèi)皮細(xì)胞)5×106cells/瓶×2
F7 Others Mouse 小鼠 Coagulation Factor VII / FVII / F7 CHO細(xì)胞裂解液 (陽(yáng)性對(duì)照)
人心肌細(xì)胞-裂解物HCM-a L
家豬皮膚細(xì)胞;SSC-S1 癌細(xì)胞，ZR-75-1細(xì)胞 NS1細(xì)胞，小鼠細(xì)胞
腺病毒轉(zhuǎn)化的人胚腎細(xì)胞;AAV-293
HA Others H5N1 甲型 H5N1 (A/chicken/Egypt/2253-1/2006) 血凝素HA1 (Hemagglutinin) 人細(xì)胞裂解液 (陽(yáng)性對(duì)照)
抗體的生物素化標(biāo)記實(shí)驗(yàn)要點(diǎn)：
1. 電壓門控鈉通道5α抗體品牌 如在反應(yīng)混合液中有疊氮鈉或游離氨基存在,會(huì)抑制標(biāo)記反應(yīng)。因此,蛋白質(zhì)在反應(yīng)前要對(duì) 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(zhì)之間的分子比按蛋白質(zhì)表面的ε-氨基的密度會(huì)有所不同,選擇不當(dāng)則影響標(biāo)記的效率,應(yīng)先用幾個(gè)不同的分子比來(lái)篩選最適條件；
3.用NHSB量過(guò)量也是不利的,抗原的結(jié)合位點(diǎn)可能因此被封閉,導(dǎo)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(shí)可加入去污劑如 Triton x-100, Tween20等；
5.當(dāng)游離ε-氨基(賴氨酸殘基的氨基)存在于抗體的抗原結(jié)合位點(diǎn)時(shí),或位于酶的催化位點(diǎn)時(shí),生物素化會(huì)降低或損傷抗體蛋白的結(jié)合力或活性；
6.生物素還可能與不同的功能基團(tuán),如羰基、氨基、巰基、異咪唑基及苯酚基,也可與糖基共價(jià)結(jié)合；
7.交聯(lián)反應(yīng)后,應(yīng)充分透析,否則,殘余的生物素會(huì)對(duì)生物素化抗體與親和素的結(jié)合產(chǎn)生競(jìng)爭(zhēng)作用；
8.在細(xì)胞的熒光標(biāo)記實(shí)驗(yàn)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(duì)某些細(xì)胞可導(dǎo)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(jià)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(jià)。不同的抗原制備的抗體,要求的效價(jià)不一。鑒定效價(jià)的方法很多,包括有試管凝集反應(yīng),瓊脂擴(kuò)散試驗(yàn),酶聯(lián)免疫吸附試驗(yàn)等。常用的抗原所制備的抗體一般都有約成的鑒定效價(jià)的方法,以資比較。如制備抗抗體的效價(jià),一般就采用瓊脂擴(kuò)散試驗(yàn)來(lái)鑒定。
2）抗體的特異性鑒定：抗體的特異性是指與相應(yīng)抗原或近似抗原物質(zhì)的識(shí)別能力?？贵w的特異性高,它的識(shí)別能力就強(qiáng)。衡量特異性通常以交叉反應(yīng)率來(lái)表示。交叉反應(yīng)率可用競(jìng)爭(zhēng)抑制試驗(yàn)測(cè)定。以不同濃度抗原和近似抗原分別做競(jìng)爭(zhēng)抑制曲線,計(jì)算各自的結(jié)合率,求出各自在IC50時(shí)的濃度,并按公式計(jì)算交叉反應(yīng)率。
如果所用抗原濃度IC50濃度為pg/管,而一些近似抗原物質(zhì)的IC50濃度幾乎是無(wú)窮大時(shí),表示這一抗血清與其他抗原物質(zhì)的交叉反應(yīng)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(jié)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(jié)合位點(diǎn)與抗原決定簇之間立體構(gòu)型的合適度決定的。有助于維持抗原抗體復(fù)合物穩(wěn)定的分子間力有氫鍵,疏水鍵,側(cè)鏈相反電荷基因的庫(kù)侖力,范德華力和空間斥力。親和力常以親和常數(shù)K表示,K的單位是L/mol?？贵w親和力的測(cè)定對(duì)抗體的篩選,確定抗體的用途,驗(yàn)證抗體的均一性等均有重要意義。
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