Anti-Hepatitis C Virus RNA-directed RNA polymerase抗体

货号： XGK0329 保存条件： 详见说明书 浓度： 1mg/1ml  应用范围： WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:50-200 形态： 详见说明书 亚型： IgG 免疫原： KLH conjugated synthetic peptide derived from Hepatitis C Virus RNA-directed RNA polymerase 适应物种： 详见说明书 宿主： 详见说明书 标记物： 详见说明书 抗体名： 丙型肝炎NS4B（65kDa）抗体 抗体英文名： Anti-Hepatitis C Virus RNA-directed RNA polymerase 保质期： 详见说明书 抗原来源： Rabbit 克隆性： 多克隆 目录编号： 详见说明书 级别： 详见说明书 靶点： 详见说明书 数量： 58 供应商： 上海西格 规格： 0.1ml/100μg  0.2ml/200μg  

一抗和二坑的区别：
抗体就是平常所说的抗体，即能和抗原特异性结合。
第二抗体是能和抗体结合的，即抗体的抗体。主要用于检测抗体的存在。
一抗是针对抗原的抗体，二抗是针对一抗的抗体。即抗体也可以充当抗原刺激机体产生抗体。也就是说，抗原进入机体刺激机体免疫系统产生免疫应答，由B细胞可以产生与相应抗原发生特异性结合的特殊蛋白质。
一抗二抗都是一种可以特异结合别的物质的基团，而且一抗可以至少结合两种其他基团（底物和二抗）。
一抗：可以特异结合底物，就是识别出我们想要检测的东西。一抗和底物结合与否用肉眼是看不出来的。
二抗：可以和一抗结合，并带有可以被检测出的标记(如带荧光、放射性、化学发光或显色基团），作用是检测一抗。 如果一抗自己带有可以被检测出的标记(如带荧光、放射性、化学发光或显色基团），则不需要二抗。但这样成本很高，因为一种一抗只识别一种底物。所以如今的设计一般是二抗带上可检测标记，再来检测一抗。而一抗识别底物。这样，当一抗结合到底物上，就可以通过二抗检测出来。 
公司专业供应的抗体，抗体是用于化学反应、分析化验、研究实验、教学实验、化学配方使用的纯净化学品，产品品质，价格实惠，多种规格供应，售后完善。

产品名称	英文名称	货号
丙型肝炎NS4B（65kDa）抗体	Anti-Hepatitis C Virus RNA-directed RNA polymerase抗体	XGK0329

英文名称  Anti-Hepatitis C Virus RNA-directed RNA polymerase
中文名称  丙型肝炎NS4B（65kDa）抗体
别    名  RNA-directed RNA polymerase; p68; RNA dependent RNA polymerase.
浓    度  1mg/1ml
规 格   0.1ml/100μg 0.2ml/200μg    
抗体来源  Rabbit
克隆类型  polyclonal
交叉反应  HCV 
产品类型  一抗
研究领域  细胞生物 细菌及
蛋白分子量  predicted molecular weight: 65kDa 
性    状  Lyophilized or Liquid 
免 疫 原   KLH conjugated synthetic peptide derived from Hepatitis C Virus RNA-directed RNA polymerase
亚    型  IgG
纯化方法   affinity purified by Protein A
储 存 液  Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4
产品应用   WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:50-200
产品介绍  HCV is a positive, single-stranded RNA virus in the Flaviviridae family. The genome is approximately 10,000 nucleotides and encodes a single polyprotein of about 3,000 amino acids. The polyprotein is processed by host cell and viral proteases into three major structural proteins, and several non-structural proteins necessary for viral replication, of which NS5B is one. NS5B RNA-dependant RNA polymerase is responsible for replication of the hepatitis C viral genome, and is currently a principal target for chemotherapeutic inhibition of HCV replication. Hepatitis C virus (HCV) can cause chronic hepatitis, cirrhosis and hepatocellular carcinoma. At present there is no vaccine effective against HCV. Host membrane insertion occurs after processing by the NS3 protease.
Function : Core protein packages viral RNA to form a viral nucleocapsid, and promotes virion budding. Modulates viral translation initiation by interacting with HCV IRES and 40S ribosomal subunit. Also regulates many host cellular functions such as signaling pathways and apoptosis. Prevents the establishment of cellular antiviral state by blocking the interferon-alpha/beta (IFN-alpha/beta) and IFN-gamma signaling pathways and by inducing human STAT1 degradation. Thought to play a role in virus-mediated cell transformation leading to hepatocellular carcinomas. Interacts with, and activates STAT3 leading to cellular transformation. May repress the promoter of p53, and sequester CREB3 and SP110 isoform 3/Sp110b in the cytoplasm. Also represses cell cycle negative regulating factor CDKN1A, thereby interrupting an important check point of normal cell cycle regulation. Targets transcription factors involved in the regulation of inflammatory responses and in the immune response: suppresses NK-kappaB activation, and activates AP-1. Could mediate apoptotic pathways through association with TNF-type receptors TNFRSF1A and LTBR, although its effect on death receptor-induced apoptosis remains controversial. Enhances TRAIL mediated apoptosis, suggesting that it might play a role in immune-mediated liver cell injury. Seric core protein is able to bind C1QR1 at the T-cell surface, resulting in down-regulation of T-lymphocytes proliferation. May transactivate human MYC, Rous sarcoma virus LTR, and SV40 promoters. May suppress the human FOS and HIV-1 LTR activity. Alters lipid metabolism by interacting with hepatocellular proteins involved in lipid accumulation and storage. Core protein induces up-regulation of FAS promoter activity, and thereby probably contributes to the increased triglyceride accumulation in hepatocytes (steatosis).E1 and E2 glycoproteins form a heterodimer that is involved in virus attachment to the host cell, virion internalization through clathrin-dependent endocytosis and fusion with host membrane. E1/E2 heterodimer binds to human LDLR, CD81 and SCARB1/SR-BI receptors, but this binding is not sufficient for infection, some additional liver specific cofactors may be needed. The fusion function may possibly be carried by E1. E2 inhibits human EIF2AK2/PKR activation, preventing the establishment of an antiviral state. E2 is a viral ligand for CD209/DC-SIGN and CLEC4M/DC-SIGNR, which are respectively found on dendritic cells (DCs), and on liver sinusoidal endothelial cells and macrophage-like cells of lymph node sinuses. These interactions allow capture of circulating HCV particles by these cells and subsequent transmission to permissive cells. DCs act as sentinels in various tissues where they entrap pathogens and convey them to local lymphoid tissue or lymph node for establishment of immunity. Capture of circulating HCV particles by these SIGN+ cells may facilitate virus infection of proximal hepatocytes and lymphocyte subpopulations and may be essential for the establishment of persistent infection.P7 seems to be a heptameric ion channel protein (viroporin) and is inhibited by the antiviral drug amantadine. Also inhibited by long-alkyl-chain iminosugar derivatives. Essential for infectivity.Protease NS2-3 is a cysteine protease responsible for the autocatalytic cleavage of NS2-NS3. Seems to undergo self-inactivation following maturation.NS3 displays three enzymatic activities: serine protease, NTPase and RNA helicase. NS3 serine protease, in association with NS4A, is responsible for the cleavages of NS3-NS4A, NS4A-NS4B, NS4B-NS and NS-NS5B. NS3/NS4A complex also prevents phosphorylation of human IRF3, thus preventing the establishment of dsRNA induced antiviral state. NS3 RNA helicase binds to RNA and unwinds dsRNA in the 3' to 5' direction, and likely RNA stable secondary structure in the template strand. Cleaves and inhibits the host antiviral protein MAVS.NS4B induces a specific membrane alteration that serves as a scaffold for the virus replication complex. This membrane alteration gives rise to the so-called ER-derived membranous web that contains the replication complex.NS is a component of the replication complex involved in RNA-binding. Its interaction with Human VAPB may target the viral replication complex to vesicles. Down-regulates viral IRES translation initiation. Mediates interferon resistance, presumably by interacting with and inhibiting human EIF2AK2/PKR. Seems to inhibit apoptosis by interacting with BIN1 and FKBP8. The hyperphosphorylated form of NS is an inhibitor of viral replication.NS5B is a RNA-dependent RNA polymerase that plays an essential role in the virus replication.Subunit : Core protein is a homomultimer that binds the C-terminal part of E1 and interacts with numerous cellular proteins. Interaction with human STAT1 SH2 domain seems to result in decreased STAT1 phosphorylation, leading to decreased IFN-stimulated gene transcription. In addition to blocking the formation of phosphorylated STAT1, the core protein also promotes ubiquitin-mediated proteasome-dependent degradation of STAT1. Interacts with, and constitutively activates human STAT3. Associates with human LTBR and TNFRSF1A receptors and possibly induces apoptosis. Binds to human SP110 isoform 3/Sp110b, HNRPK, C1QR1, YWHAE, UBE3A/E6AP, DDX3X, APOA2 and RXRA proteins. Interacts with human CREB3 nuclear transcription protein, triggering cell transformation. May interact with human p53. Also binds human cytokeratins KRT8, KRT18, KRT19 and VIM (vimentin). E1 and E2 glycoproteins form a heterodimer that binds to human LDLR, CLDN1, CD81 and SCARB1 receptors. E2 binds and inhibits human EIF2AK2/PKR. Also binds human CD209/DC-SIGN and CLEC4M/DC-SIGNR. p7 forms a homoheptamer in vitro. NS2 forms a homodimer containing a pair of composite active sites at the dimerization interface. NS2 seems to interact with all other non-structural (NS) proteins. NS4A interacts with NS3 serine protease and stabilizes its folding. NS3-NS4A complex is essential for the activation of the latter and allows membrane anchorage of NS3. NS3 interacts with human TANK-binding kinase TBK1 and MAVS. NS4B and NS form homodimers and seem to interact with all other non-structural (NS) proteins. NS also interacts with human EIF2AK2/PKR, FKBP8, GRB2, BIN1, PIK3R1, SRCAP, VAPB and with most Src-family kinases. NS5B is a homooligomer and interacts with human VAPB, HNRNPA1 and SEPT6.Subcellular Location : RNA-directed RNA polymerase: Host endoplasmic reticulum membrane; Single-pass type I membrane protein (Potential). Note=Host membrane insertion occurs after processing by the NS3 protease.Post-translational modifications : Specific enzymatic cleavages in vivo yield mature proteins. The structural proteins, core, E1, E2 and p7 are produced by proteolytic processing by host signal peptidases. The core protein is synthesized as a 21 kDa precursor which is retained in the ER membrane through the hydrophobic signal peptide. Cleavage by the signal peptidase releases the 19 kDa mature core protein. The other proteins (p7, NS2-3, NS3, NS4A, NS4B, NS and NS5B) are cleaved by the viral proteases.Envelope E1 and E2 glycoproteins are highly N-glycosylated.Core protein is phosphorylated by host PKC and PKA.NS is phosphorylated in a basal form termed p56. p58 is an hyperphosphorylated form of p56. p56 and p58 coexist in the cell in roughly equivalent amounts. Hyperphosphorylation is dependent on the presence of NS4A. Human AKT1, RPS6KB1/p70S6K, MAP2K1/MEK1, MAP2K6/MKK6 and CSNK1A1/CKI-alpha kinases may be responsible for NS phosphorylation.NS4B is palmitoylated. This modification may play a role in its polymerization or in protein-protein interactions.The N-terminus of a fraction of NS4B molecules seems to be relocated post-translationally from the cytoplasm to the ER lumen, with a 5th transmembrane segment. The C-terminus of NS2 may be lumenal with a fourth transmembrane segment.Core protein is ubiquitinated; mediated by UBE3A and leading to core protein subsequent proteasomal degradation.Similarity : Belongs to the hepacivirus polyprotein family.Contains 1 helicase ATP-binding domain.Contains 1 peptidase C18 domain.Contains 1 peptidase S29 domain.Contains 1 RdRp catalytic domain.丙型肝炎发病机理仍未十分清楚，当HCV在肝细胞内复制引起肝细胞结构和功能改变或干扰肝细胞蛋白合成，可造成肝细胞变性坏死，表明HCV直接损害肝脏，导致发病起一定作用。但多数学者认为细胞免疫病理反应可能起重要作用，发现肝炎与乙型肝炎一样，其组织浸润细胞以CD3+为主，细胞毒T细胞（TC）特异攻击HCV感染的靶细胞，可引起肝细胞损伤。

抗体的生物素化标记实验要点：
1.如在反应混合液中有或游离氨基存在,会YZ标记反应。因此,蛋白质在反应前要对 0.1mol/L碳酸氢钠缓冲液或0.5mol/L硼酸缓冲液充分透析；
2.所用的NHSB及待生物素化蛋白质之间的分子比按蛋白质表面的ε-氨基的密度会有所不同,选择不当则影响标记的效率,应先用几个不同的分子比来筛选Z适条件；
3.用NHSB量过量也是不利的,抗原的结合位点可能因此被封闭,导致抗体失活；
4.由于抗体的氨基不易接近可能造成生物素化不足,此时可加入去污剂如 Triton x-100, Tween20等；
5.当游离ε-氨基(赖氨酸残基的氨基)存在于抗体的抗原结合位点时,或位于酶的催化位点时,生物素化会降低或损伤抗体蛋白的结合力或活性；
6.生物素还可能与不同的功能基团,如羰基、氨基、巯基、异咪唑基及苯酚基,也可与糖基共价结合；
7.交联反应后,应充分透析,否则,残余的生物素会对生物素化抗体与亲和素的结合产生竞争作用；
8.在细胞的荧光标记实验中,中和亲和素的本底低,但由于链霉亲和素含有少量正电荷,故对某些细胞可导致高本底。
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抗体的制备过程：
1. 免疫原的制备
普通的大分子蛋白，通过分子克隆构建载体并在大肠杆菌中进行诱导表达获得重组蛋白，纯化鉴定后可直接作为免疫原。
小分子蛋白或化合物等分子量小，需要偶联载体对该分子进行改造才能使其成为具有免疫原性的抗原，常见偶联载体如BSA、OVA、HAS等。
2. 免疫动物
常用于制备抗血清的动物有豚鼠、家兔、鸡、大小鼠等，大量生产时需要用到狗、绵羊、山羊等。
3. 免疫血清的收集
一般家兔、绵羊、山羊可采用静动脉采血，家兔、豚鼠、大鼠、鸡可采用心脏采血，家兔、山羊、绵羊可采用静脉采血。
4. 免疫血清的纯化与鉴定
得到的抗血清需要进一步的纯化，利用偶联了抗原的亲和柱进行层析，具有GX，特异性强，纯度高的特定。接着要鉴定纯化蛋白的含量、相对分子的质量、纯度以及特异性。
5. 免疫血清的保存
建议将Anti-Hepatitis C Virus RNA-directed RNA polymerase抗体分装后进行保存。抗体一般比较稳定，在-80℃ ～-20 ℃可以保存约5年而不会影响效价，而真空干燥保存时间可以更久。保存前需经CJ并添加防腐剂。