An apoptotic inducer, aralin, is a novel type II ribosome-inactivating protein from Aralia elata

Verfasser / Beitragende:
[Makoto Tomatsu, Toshiya Kondo, Takafumi Yoshikawa, Takashi Komeno, Naomi Adachi, Yasushi Kawasaki, Akira Ikuta, Fumio Tashiro]
Ort, Verlag, Jahr:
2004
Enthalten in:
Biological Chemistry, 385/9(2004-09-01), 819-827
Format:
Artikel (online)
ID: 378883992
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024 7 0 |a 10.1515/BC.2004.107  |2 doi 
035 |a (NATIONALLICENCE)gruyter-10.1515/BC.2004.107 
245 0 3 |a An apoptotic inducer, aralin, is a novel type II ribosome-inactivating protein from Aralia elata  |h [Elektronische Daten]  |c [Makoto Tomatsu, Toshiya Kondo, Takafumi Yoshikawa, Takashi Komeno, Naomi Adachi, Yasushi Kawasaki, Akira Ikuta, Fumio Tashiro] 
520 3 |a We recently found that aralin, a novel cytotoxic protein consisting of two subunits, from Aralia elata selectively induces apoptosis in transformed cells as compared to normal cells. Here we report that aralin is a lectin specific for galactose (Gal) and its derivatives, and possesses RNA N-glycosidase activity as a new type II ribosome-inactivating protein (RIP). The RNA N-glycosidase activity of aralin was detected in cell-free and whole cell systems by the generation of an R-fragment from 28S rRNA. Coinciding with appearance of the R-fragment in aralin-treated cells, significant inhibition of protein synthesis was observed prior to the onset of apoptosis. Aralin-evoked cell death was efficiently repressed by the addition of Gal and its derivatives. Interestingly, melibiose preferentially protected normal cells from apoptosis as compared with transformed cells. Using rhodamine-coupled aralin, the aralin receptor could be clearly detected around the cell surface of transformed cells, but to a lesser extent on normal cells. Receptor binding was suppressed by Gal. These results indicate that aralin is incorporated into cells via its Gal-containing cell surface receptor and induces apoptosis through its RIP activity. Moreover, the expression level and/or structural changes of the aralin receptor may affect the sensitivity toward aralin. 
540 |a © Walter de Gruyter 
690 7 |a Biochemistry  |2 nationallicence 
690 7 |a Molecular biology  |2 nationallicence 
690 7 |a Cellular biology  |2 nationallicence 
690 7 |a apoptosis  |2 nationallicence 
690 7 |a aralin  |2 nationallicence 
690 7 |a cytotoxic protein  |2 nationallicence 
690 7 |a lectin  |2 nationallicence 
690 7 |a ribosome-inactivating protein (RIP)  |2 nationallicence 
690 7 |a RNA N-glycosidase  |2 nationallicence 
700 1 |a Tomatsu  |D Makoto  |u Akita Research Institute of Food and Brewing (ARIF), Arayamachi, Akita 010-1623, Japan  |4 aut 
700 1 |a Kondo  |D Toshiya  |u School of Pharmaceutical Sciences, Kitasato University, Minato-ku, Tokyo 108-8641, Japan  |4 aut 
700 1 |a Yoshikawa  |D Takafumi  |u School of Pharmaceutical Sciences, Kitasato University, Minato-ku, Tokyo 108-8641, Japan  |4 aut 
700 1 |a Komeno  |D Takashi  |u Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
700 1 |a Adachi  |D Naomi  |u Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
700 1 |a Kawasaki  |D Yasushi  |u Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
700 1 |a Ikuta  |D Akira  |u Research Institute for Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
700 1 |a Tashiro  |D Fumio  |u Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
773 0 |t Biological Chemistry  |d Walter de Gruyter  |g 385/9(2004-09-01), 819-827  |x 1431-6730  |q 385:9<819  |1 2004  |2 385  |o bchm 
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950 |B NATIONALLICENCE  |P 700  |E 1-  |a Tomatsu  |D Makoto  |u Akita Research Institute of Food and Brewing (ARIF), Arayamachi, Akita 010-1623, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Kondo  |D Toshiya  |u School of Pharmaceutical Sciences, Kitasato University, Minato-ku, Tokyo 108-8641, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Yoshikawa  |D Takafumi  |u School of Pharmaceutical Sciences, Kitasato University, Minato-ku, Tokyo 108-8641, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Komeno  |D Takashi  |u Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Adachi  |D Naomi  |u Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Kawasaki  |D Yasushi  |u Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Ikuta  |D Akira  |u Research Institute for Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Tashiro  |D Fumio  |u Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 773  |E 0-  |t Biological Chemistry  |d Walter de Gruyter  |g 385/9(2004-09-01), 819-827  |x 1431-6730  |q 385:9<819  |1 2004  |2 385  |o bchm 
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