1.
図書 |
平田肇, 茂木立志担当編集
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2.
図書 |
高橋泰常編
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3.
図書 |
R. W. ヘンドラー著 ; 安楽泰宏, 丸山博巳, 二井将光共訳
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4.
図書 |
G.M.W. Cook, R.W. Stoddart著 ; 内海耕慥監訳
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5.
図書 |
井上章, 品川嘉也編
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6.
図書 |
阿部康次, 土田英俊著
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7.
図書 |
名倉宏 [ほか] 編集
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8.
図書 |
西田泰伸著
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9.
図書 |
井上章,品川嘉也編
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10.
論文(リポジトリ) |
福田, 剛明 ; 柿原, 敏夫 ; 山田, 俊幸
概要:
We have established human leukemic cell lines, designated as KY-Ra and KY-Rb, which are highly resistant for cytosine ar
…
abinoside (AraC) and behenosyl AraC. Intercellular AraC increased in proportion to incubation time in parental KY-821, whereas did not increase in resistant cell lines. Intracellular AraC excluded in the extracellular medium in short time on KY-Ra and KY-Rb. Activity of deoxycytidine kinase was not so different in each cell line. We also obtained one hybridoma which secretes an antibody reacting with only resistant cell lines, although definite characterization has yet determined. NNatural IL-1, INFγ, and TNFα inhibited the proliferation of KY-821. In contrast natural IL-1 promoted ^3H-thymidine uptake of KY-Ra and KY-Rb, and no suppressive effect of IFNγ and TNFα was observed in other cell lines. These results indicate that AraC efflux was attributable to unknown membrane protein probably distinct from P-glycoprotein and a different reactivity between resistant and non-resistant cell lines for growth factors is also owing to some changes of cell membrane.
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