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Yoshiaki Kamada

Researcher at National Institute for Basic Biology, Japan

Publications -  35
Citations -  8098

Yoshiaki Kamada is an academic researcher from National Institute for Basic Biology, Japan. The author has contributed to research in topics: Autophagy & Atg1. The author has an hindex of 24, co-authored 35 publications receiving 7621 citations. Previous affiliations of Yoshiaki Kamada include Graduate University for Advanced Studies & Johns Hopkins University.

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Dynamics and diversity in autophagy mechanisms: lessons from yeast

TL;DR: The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today.
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Tor-Mediated Induction of Autophagy via an Apg1 Protein Kinase Complex

TL;DR: It is shown that the protein kinase activity of Apg1 is enhanced by starvation or rapamycin treatment, and it is found that Apg13, which binds to and activates ApG1, is hyperphosphorylated in a Tor-dependent manner, reducing its affinity to Apg 1.
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The pre-autophagosomal structure organized by concerted functions of APG genes is essential for autophagosome formation.

TL;DR: Based on Apg protein localization, a novel structure that functions in autophagosome formation is identified and it is revealed that the formation of both a phosphatidylethanolamine‐conjugated Aut7p and an Apg12p–Apg5p conjugate is essential for the localization of Aut 7p to the pre‐autophagosomal structure.
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The protein kinase C-activated MAP kinase pathway of Saccharomyces cerevisiae mediates a novel aspect of the heat shock response.

TL;DR: It is proposed that the heat-induced signal for pathway activation is generated in response to weakness in the cell wall created during growth under thermal stress, perhaps as a result of increased membrane fluidity.
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Tor directly controls the Atg1 kinase complex to regulate autophagy.

TL;DR: It is suggested that the direct control of the Atg1 complex by TORC1 induces autophagy, and expression of an unphosphorylatable Atg13 mutant bypasses theTORC1 pathway to induce autophagic through activation of Atg2 in cells growing under nutrient-rich conditions.