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FITC標記的腺苷酸激酶抗體

文字:[大][中][小] 2017-5-3    瀏覽次數(shù):1162    

                                   FITC標記的腺苷酸激酶抗體                                                                                                                                                
英文名稱Anti-ADK/FITC
中文名稱:FITC標記的腺苷酸激酶抗體
別    名Adenosine kinase; AK; 5033405D03Rik; AI255373; AI987814; MGC6593; 2310026J05Rik; Adenosine 5'-phosphotransferase; OTTHUMP00000019864; OTTHUMP00000019865; ADK_HUMAN; Adenosine kinase; AK; Full=Adenosine 5'-phosphotransferase.  

詳細介紹:


規(guī)格:100ul 
說 明 書100ul  
研究領(lǐng)域激酶和磷酸酶  
抗體來源Rabbit
克隆類型Polyclonal
交叉反應 Human, Mouse, Rat, Chicken, Dog, Pig, Cow, 
產(chǎn)品應用IF=1:50-200  
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量41kDa
性    狀Lyophilized or Liquid
濃    度1mg/ml
免 疫 原KLH conjugated synthetic peptide derived from human ADK/adenylate kinase
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.

相關(guān)資料:


產(chǎn)品介紹background:
widespread effects on the cardiovascular, nervous, respiratory, and immune systems and inhibitors of ADK could play an important pharmacological role in increasing intravascular adenosine concentrations and acting as antiinflammatory agents. The encoded protein does not present any sequence similarities to other well characterized mammalian nucleoside kinases. In contrast, 2 regions were identified with significant sequence identity to microbial ribokinase and fructokinases and a bacterial inosine/guanosine kinase. Thus, ADK is a structurally distinct mammalian nucleoside kinase that appears to be akin to sugar kinases of microbial origin. Animal studies have demonstrated that a deficiency of adenosine metabolism a powerful contributor to the development of neonatal hepatic steatosis, providing a model for the rapid development of postnatally lethal fatty liver.

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