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Hitoshi Nakatogawa

Researcher at Tokyo Institute of Technology

Publications -  76
Citations -  18888

Hitoshi Nakatogawa is an academic researcher from Tokyo Institute of Technology. The author has contributed to research in topics: Autophagy & ATG8. The author has an hindex of 36, co-authored 70 publications receiving 15280 citations. Previous affiliations of Hitoshi Nakatogawa include National Presto Industries & Graduate University for Advanced Studies.

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Journal ArticleDOI

Control of SecA and SecM translation by protein secretion

Hitoshi Nakatogawa, +2 more
- 01 Apr 2004 - 
TL;DR: Evidence suggests that elongation-arresting SecM has a role of upregulating the functionality of newly synthesized SecA molecules, presumably by bringing the mRNA to the vicinity of the membrane/Sec translocation apparatus.
Journal ArticleDOI

COPII vesicles contribute to autophagosomal membranes

Takayuki Shima, +2 more
- 06 May 2019 - 
TL;DR: This study provides a definitive answer to a long-standing, fundamental question regarding the mechanisms of autophagosome formation by implicating COPII vesicles as a membrane source for autphagosomes.
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Translation arrest of SecM is essential for the basal and regulated expression of SecA

Akiko Murakami, +2 more
- 17 Aug 2004 - 
TL;DR: The SecM protein of Escherichia coli contains an arrest sequence, which interacts with the ribosomal exit tunnel to halt translation elongation beyond Pro-166, and has at least two roles in SecA translation, which is required for the synthesis of SecA at levels sufficient to support cell growth.
Journal Article

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2459 more
- 01 Jan 2016 - 
Journal ArticleDOI

Reticulophagy and nucleophagy: New findings and unsolved issues.

Hitoshi Nakatogawa, +1 more
- 13 Nov 2015 - 
TL;DR: The recent study revealed that yeast cells actively degrade the endoplasmic reticulum and even part of the nucleus via selective autophagy under nitrogen-deprived conditions, and identified novel receptors, Atg39 and Atg40, specific to these pathways.