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冠狀病毒刺突糖蛋白抗體

參   考   價: 13

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品       牌Abcam

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更新時間:2015-06-12 11:05:59瀏覽次數(shù):475次

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冠狀病毒刺突糖蛋白抗體
WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500 (石蠟切片需做抗原修復)
not yet tested in other applications.

冠狀病毒刺突糖蛋白抗體

英文名稱 SARS spike glycoprotein
中文名稱 冠狀病毒刺突糖蛋白抗體
別    名 E2; E2 glycoprotein; Human coronavirus spike glycoprotein; Peplomer protein; S; S glycoprotein; SPIKE_CVHSA; Severe acute respiratory syndrome spike glycoprotein; Severe acute respiratory syndrome virus spike glycoprotein; Spike glycoprotein; VGL2.

說 明 書 0.2ml  
研究領域 細胞生物  細菌及病毒  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 SARS virus
產品應用 WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500 (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.
分 子 量 138kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/1ml
免 疫 原 KLH conjugated synthetic peptide derived from human SARS spike glycoprotein
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
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.

PubMed PubMed
產品介紹 background:
A novel coronavirus has been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive stranded RNA approximay 27 to 31kb in length. SARS infection can be mediated by the binding of the viral spike protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin converting enzyme 2 (ACE2) on target cells. This binding can be blocked by a soluble form of ACE2. 

Function:
S1 attaches the virion to the cell membrane by interacting with human ACE2 and CLEC4M/DC-SIGNR, initiating the infection. Binding to the receptor and internalization of the virus into the endosomes of the host cell probably induces conformational changes in the S glycoprotein. Proteolysis by cathepsin CTSL may unmask the fusion peptide of S2 and activate membranes fusion within endosomes. 
S2 is a class I viral fusion protein. Under the current model, the protein has at least three conformational states: pre-fusion native state, pre-hairpin intermediate state, and post-fusion hairpin state. During viral and target cell membrane fusion, the coiled coil regions (heptad repeats) assume a trimer-of-hairpins structure, positioning the fusion peptide in close proximity to the C-terminal region of the ectodomain. The formation of this structure appears to drive apposition and subsequent fusion of viral and target cell membranes.
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