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Takeshi Kaizuka

Researcher at University of Tokyo

Publications -  17
Citations -  3056

Takeshi Kaizuka is an academic researcher from University of Tokyo. The author has contributed to research in topics: Autophagy & Autophagy-related protein 13. The author has an hindex of 9, co-authored 13 publications receiving 2558 citations. Previous affiliations of Takeshi Kaizuka include Tokyo Medical and Dental University.

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Nutrient-dependent mTORC1 Association with the ULK1–Atg13–FIP200 Complex Required for Autophagy

TL;DR: A novel mammalian autophagy factor, Atg13, is reported, which forms a stable approximately 3-MDa protein complex with ULK1 and FIP200, and suggests that mTORC1 suppressesAutophagy through direct regulation of the approximately 3,MDa ULK 1-Atg13-FIP200 complex.
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An Autophagic Flux Probe that Releases an Internal Control

TL;DR: The GFP- LC3-RFP-LC3ΔG probe is a simple and quantitative method to evaluate autophagic flux in cultured cells and whole organisms, and re-evaluated previously reported autophagy-modulating compounds, performed a high-throughput screen of an approved drug library, and identified autophile modulators.
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Tti1 and Tel2 Are Critical Factors in Mammalian Target of Rapamycin Complex Assembly

TL;DR: This study identified KIAA0406 as a novel mTOR-interacting protein that has sequence homology with Schizosaccharomyces pombe Tti1 and confirmed that Tti 1 binds to Tel2 also in mammalian cells, and Tti2 interacts with and stabilizes all six members of the PIKK family of proteins.
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Dynamic association of the ULK1 complex with omegasomes during autophagy induction.

TL;DR: It is shown that the ULK1 complex colocalises with omegasomes in a PtdIns3P-dependent way, and a complete sequence of steps leading to autophagosome formation is established for the first time.
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FIP200 regulates targeting of Atg16L1 to the isolation membrane

TL;DR: It is found that FIP200, which is involved in proximal events, directly interacts with Atg16L1, one of the downstream Atg factors, in an Atg14‐ and phosphatidylinositol 3‐kinase‐independent manner.