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Start Over Author "Ichijo, Hidenori" Journal molecular cell
7 results on '"Ichijo, Hidenori"'

4. Essential Role of E2-25K/Hip-2 in Mediating Amyloid-β Neurotoxicity

Author

Song, Sungmin, primary, Kim, So-Young, additional, Hong, Yeon-Mi, additional, Jo, Dong-Gyu, additional, Lee, Joo-Yong, additional, Shim, Sang Mi, additional, Chung, Chul-Woong, additional, Seo, Soo Jung, additional, Yoo, Yung Joon, additional, Koh, Jae-Young, additional, Lee, Min Chul, additional, Yates, Allan J, additional, Ichijo, Hidenori, additional, and Jung, Yong-Keun, additional

Published
2003
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6. ASK1 Is Essential for JNK/SAPK Activation by TRAF2

Author

Nishitoh, Hideki, primary, Saitoh, Masao, additional, Mochida, Yoshiyuki, additional, Takeda, Kohsuke, additional, Nakano, Hiroyasu, additional, Rothe, Mike, additional, Miyazono, Kohei, additional, and Ichijo, Hidenori, additional

Published
1998
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7. Essential role of E2-25K/Hip-2 in mediating amyloid-beta neurotoxicity.

Author

Song S, Kim SY, Hong YM, Jo DG, Lee JY, Shim SM, Chung CW, Seo SJ, Yoo YJ, Koh JY, Lee MC, Yates AJ, Ichijo H, and Jung YK

Subjects
Aged, Aged, 80 and over, Alzheimer Disease genetics, Amyloid beta-Peptides toxicity, Animals, Apoptosis genetics, Brain pathology, Brain physiopathology, Cells, Cultured, Cysteine Endopeptidases metabolism, Female, Fetus, Gene Expression Regulation, Enzymologic physiology, Humans, JNK Mitogen-Activated Protein Kinases, Ligases genetics, MAP Kinase Kinase Kinase 5, MAP Kinase Kinase Kinases metabolism, Mice, Mice, Transgenic, Mitogen-Activated Protein Kinases metabolism, Multienzyme Complexes metabolism, Mutation genetics, Neurons pathology, Peptide Fragments metabolism, Peptide Fragments toxicity, Proteasome Endopeptidase Complex, Rats, Ubiquitin genetics, Ubiquitin metabolism, Up-Regulation drug effects, Alzheimer Disease enzymology, Amyloid beta-Peptides metabolism, Brain enzymology, Ligases metabolism, Neurons enzymology, Ubiquitin-Conjugating Enzymes, Up-Regulation physiology
Abstract

The ubiquitin/proteasome system has been proposed to play an important role in Alzheimer's disease (AD) pathogenesis. However, the critical factor(s) modulating both amyloid-beta peptide (Abeta) neurotoxicity and ubiquitin/proteasome system in AD are not known. We report the isolation of an unusual ubiquitin-conjugating enzyme, E2-25K/Hip-2, as a mediator of Abeta toxicity. The expression of E2-25K/Hip-2 was upregulated in the neurons exposed to Abeta(1-42) in vivo and in culture. Enzymatic activity of E2-25K/Hip-2 was required for both Abeta(1-42) neurotoxicity and inhibition of proteasome activity. E2-25K/Hip-2 functioned upstream of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal kinase (JNK) in Abeta(1-42) toxicity. Further, the ubiquitin mutant, UBB+1, a potent inhibitor of the proteasome which is found in Alzheimer's brains, was colocalized and functionally interacted with E2-25K/Hip-2 in mediating neurotoxicity. These results suggest that E2-25K/Hip-2 is a crucial factor in regulating Abeta neurotoxicity and could play a role in the pathogenesis of Alzheimer's disease.

Published
2003
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