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Tomoki Chiba

Researcher at University of Tsukuba

Publications -  120
Citations -  27820

Tomoki Chiba is an academic researcher from University of Tsukuba. The author has contributed to research in topics: Ubiquitin & Ubiquitin ligase. The author has an hindex of 52, co-authored 110 publications receiving 25162 citations. Previous affiliations of Tomoki Chiba include New Energy and Industrial Technology Development Organization & Institute of Medical Science.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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An nrf2/small maf heterodimer mediates the induction of phase ii detoxifying enzyme genes through antioxidant response elements

TL;DR: It is demonstrated that Nrf2 is essential for the transcriptional induction of phase II enzymes and the presence of a coordinate transcriptional regulatory mechanism for phase II enzyme genes and the nrf2-deficient mice may prove to be a very useful model for the in vivo analysis of chemical carcinogenesis and resistance to anti-cancer drugs.
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Loss of autophagy in the central nervous system causes neurodegeneration in mice

TL;DR: It is found that mice lacking Atg7 specifically in the central nervous system showed behavioural defects, including abnormal limb-clasping reflexes and a reduction in coordinated movement, and died within 28 weeks of birth, and that impairment of autophagy is implicated in the pathogenesis of neurodegenerative disorders involving ubiquitin-containing inclusion bodies.
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Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice

TL;DR: Conditional knockout mice of Atg7 were generated and showed the important role of autophagy in starvation response and the quality control of proteins and organelles in quiescent cells.
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Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase

TL;DR: The findings indicate that accumulation of proteins that have yet to be identified causes a selective neural cell death without formation of Lewy bodies, and should enhance the exploration of the molecular mechanisms of neurodegeneration in Parkinson disease as well as in other Neurodegenerative diseases that are characterized by involvement of abnormal protein ubiquitination.