Author

J.-i. Sakamaki

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 4

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:development & morphogenesis· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

N. Mizushima· 2 shared A. E. Davis· 1 shared A. Newcombe· 1 shared A.-L. Latif· 1 shared B. Higgens· 1 shared C. Iorio· 1 shared C. McKeeve· 1 shared C. Reid· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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2 shared papersCell Biology

N. Mizushima

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4 papers

Recent·Most cited

Syntaxin 17 recruitment to mature autophagosomes is temporally regulated by PI4P accumulation

S. Shinoda, Y. Sakai, T. Matsui, M. Uematsu, I. Koyama-Honda, J.-i. Sakamaki, H. Yamamoto, N. Mizushima

The paper shows that STX17 recruitment to mature autophagosomes is temporally regulated by PI4P-driven changes in membrane charge.

bioRxiv · Sep 11, 2023Cell Biology

The pH-sensing Rim101 pathway regulates cell size in budding yeast

M. Shimasawa, J.-i. Sakamaki, N. Mizushima

The paper identifies Rim21 as a positive regulator of cell size in budding yeast through the Rim101 pathway, showing its role in size regulation under physiological conditions and alkaline stress.

bioRxiv · Jul 3, 2022Cell Biology

Role of the G-Protein Coupled Receptor 3-Salt Inducible Kinase 2 Pathway in Human β CellProliferation

C. Iorio, J. L. Rourke, L. Wells, J.-I. Sakamaki, E. Moon, Q. Hu, T. Kin, R. Screaton

This study identifies the GPR3-SIK2 pathway as a regulator of human β cell proliferation, showing that GPR3 silencing activates SIK2 to drive cell cycle entry and increase β cell mass.

bioRxiv · May 31, 2021Cell Biology

BRD4-mediated repression of p53 is a target for combination therapy in AML

A.-L. Latif, A. Newcombe, S. Li, K. Gilroy, N. Robertson, X. Lei, H. Stewart, J. Cole, M. T. Terradas, L. Rishi, L. McGarry, C. McKeeve, C. Reid, W. Clark, J. Campos, , P. D. Adams

This study shows that combining MDM2 inhibitors and BET inhibitors synergistically kills AML cells by enhancing p53 activation through BRD4's repressive function.

bioRxiv · Sep 16, 2020Cell Biology