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丙肝病毒核心抗原C区抗体,Anti-HCV Core protein抗体

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“丙肝病毒核心抗原C区抗体,Anti-HCV Core protein抗体”我公司拥有领先的细胞服务技术,先进的仪器设备和专业的ELISA检测试剂盒、生物索标记、荧光索标记、酶标记等,广泛用于多种分析研究与技术测定。欢迎来电咨询,我们将竭诚为你服务!

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产品名称  丙肝病毒核心抗原C区抗体,Anti-HCV Core protein抗体                                             
产品编号 BYk-0221R   

相关标记 HRP Biotin Gold RBITC AP FITC Cy3 Cy5 Cy5.5 Cy7 PE PE-Cy3 PE-Cy5 PE-Cy5.5
PE-CY7 APC Alexa Fluor 350 Alexa Fluor 488 Alexa Fluor 555 Alexa Fluor 647
浓 度 1mg/1ml
抗体来源 Rabbit OR MOUSE
克隆类型 polyclonal or monoclonal
产品类型 一抗
产品用途  科研实验,用于免疫组化实验,WB实验、IF、IP、ELISA实验,相应的标记抗体有HRP标记抗体,FITC标记,BIO等。
性 状 Lyophilized or Liquid
亚 型 IgG  
   

丙肝病毒核心抗原C区抗体,Anti-HCV Core protein抗体保存条件 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.

丙肝病毒核心抗原C区抗体,Anti-HCV Core protein抗体产品说明:

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. Plays an important 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 isoform3/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. Mediates apoptotic pathways throught association with TNF-type receptors TNFRSF1A and LTBR, although its effect on death receptors-induced apoptosis remains controvertial. Enhances TRAIL mediated apoptosis, suggesting that it might play a role in mediated apoptosis, suggesting that it might play a role in immune-mediated liver cell injury. Secreted 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. May alter lipid metabolism by interacting with hepatocellular proteins involved in lipid accumulation and storage.


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