Tomoko Taguchi
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Tomoko Taguchi has a total of 21 co-authors. Here are the top co-authors by number of shared publications:
Hajime Okita
Department of Developmental Biology, National Research Institute for Child Health and Development, Setagaya-ku, Tokyo
1 shared publicationHideki Nakajima
Department of Pathology, National Children's Medical Research Center , Setagaya-ku, Tokyo
1 shared publicationHiroshi Nakao
Department of Infectious Diseases Research, National Children's Medical Research Center , Setagaya-ku, Tokyo
1 shared publicationHisami Takenouchi
Department of Developmental Biology, National Research Institute for Child Health and Development, Setagaya-ku, Tokyo
1 shared publicationJun Matsui
Department of Developmental Biology, National Research Institute for Child Health and Development, Setagaya-ku, Tokyo
1 shared publicationJunichiro Fujimoto
Department of Developmental Biology, National Research Institute for Child Health and Development, Setagaya-ku, Tokyo
1 shared publication
Latest Publications
- 1 April 2006
- Published by Elsevier in Experimental Hematology
- Vol. 34 (4) , 508-518
Involvement of insulin-like growth factor-I and insulin-like growth factor binding proteins in pro–B-cell development
- 1 April 2006
- Published by Elsevier in Experimental Hematology
- Vol. 34 (4) , 508-518
Involvement of insulin-like growth factor-I and insulin-like growth factor binding proteins in pro–B-cell development
- Open Access
- 15 March 2002
- Published by Oxford University Press (OUP) in The Journal of Infectious Diseases
- Vol. 185 (6) , 785-796
Inhibition of Shiga Toxin Cytotoxicity in Human Renal Cortical Epithelial Cells by Nitrobenzylthioinosine
Nitrobenzylthioinosine (NBTI), a nucleoside-transport inhibitor, has been found to possess the ability to prevent the cytotoxic action of Shiga toxin (Stx) 1 in human renal cortical epithelial cells (HRCECs), thereby protecting HRCECs from cell death. Further examination revealed that NBTI does not affect either the binding or the endocytosis of Stx1 but alters the intracellular transport of Stx1. Generally, endocytosed Stx1 is thought to be transported from endosomes to the endoplasmic reticulum. In NBTI-treated cells, however, the endocytosed Stx1 is delivered to an early endosome, but no further transportation occurs. Moreover, Stx1 is rapidly excreted from NBTI-treated HRCECs, preventing the accumulation of Stx1. Investigation of the NBTI-mediated protection mechanism against Stx cytotoxicity may provide insights into the analysis of Stx-mediated cell damage and lead to improvements in therapeutic approaches for diseases caused by Stx.
- 15 March 2002
- Published by Oxford University Press (OUP) in The Journal of Infectious Diseases
- Vol. 185 (6) , 785-796
Open AccessInhibition of Shiga Toxin Cytotoxicity in Human Renal Cortical Epithelial Cells by Nitrobenzylthioinosine
Nitrobenzylthioinosine (NBTI), a nucleoside-transport inhibitor, has been found to possess the ability to prevent the cytotoxic action of Shiga toxin (Stx) 1 in human renal cortical epithelial cells (HRCECs), thereby protecting HRCECs from cell death. Further examination revealed that NBTI does not affect either the binding or the endocytosis of Stx1 but alters the intracellular transport of Stx1. Generally, endocytosed Stx1 is thought to be transported from endosomes to the endoplasmic reticulum. In NBTI-treated cells, however, the endocytosed Stx1 is delivered to an early endosome, but no further transportation occurs. Moreover, Stx1 is rapidly excreted from NBTI-treated HRCECs, preventing the accumulation of Stx1. Investigation of the NBTI-mediated protection mechanism against Stx cytotoxicity may provide insights into the analysis of Stx-mediated cell damage and lead to improvements in therapeutic approaches for diseases caused by Stx.