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タイトル: Control of hypoxia-induced tumor cell adhesion by cytophilic human catalase.
著者: Yata, Tomoya
Nishikawa, Makiya  kyouindb  KAKEN_id
Nishizaki, Chika
Oku, Masahide  kyouindb  KAKEN_id
Yurimoto, Hiroya  kyouindb  KAKEN_id
Sakai, Yasuyoshi  kyouindb  KAKEN_id
Takakura, Yoshinobu  kyouindb  KAKEN_id
著者名の別形: 西川, 元也
キーワード: Abnormal cell adhesion
Free radicals
Hypoxia
Reactive oxygen species
Recombinant human catalase
発行日: 15-Dec-2009
出版者: Elsevier
誌名: Free radical biology & medicine
巻: 47
号: 12
開始ページ: 1772
終了ページ: 1778
抄録: Hypoxia-induced reactive oxygen species (ROS)-mediated expression of a variety of genes in endothelial cells has been suggested to be involved in abnormal cell adhesion. To prevent this by accelerated binding of catalase to endothelial cells, human catalase (hCAT), an enzyme catalyzing the decomposition of hydrogen peroxide, was fused with three repeats of arginine-glycine-aspartic acid peptide or nona arginine peptide at the C-terminal to obtain hCAT-(RGD)3 and hCAT-R9, respectively. Human CAT and its derivatives were expressed in yeast Pichia pastoris and purified. The specific activity and secondary structure of hCAT-(RGD)3 and hCAT-R9 were close to those of hCAT, but these derivatives showed higher binding to the mouse aortic vascular endothelial cell line MAEC than hCAT, indicating that they are cytophilic derivatives. Hypoxic treatment of MAEC increased the intracellular ROS level, the binding of mouse melanoma cells, and the activity of transcription factors, hypoxia inducible factor-1 and nuclear factor-kappaB. hCAT-(RGD)3 or hCAT-R9 efficiently inhibited these changes compared with hCAT. These results indicate that cytophilic hCAT-(RGD)3 and hCAT-R9 are effective in inhibiting hypoxia-induced tumor cell adhesion to endothelial cells.
著作権等: c 2009 Elsevier Inc. All rights reserved.
This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
URI: http://hdl.handle.net/2433/91262
DOI(出版社版): 10.1016/j.freeradbiomed.2009.09.027
PubMed ID: 19804819
出現コレクション:学術雑誌掲載論文等

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