Author

S. Takao

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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Cancer Biology· 3 Plant Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:cancer & tumor microenvironment· 3 Organism:human· 3 Organism:Arabidopsis· 1 Assay:bulk RNA-seq· 1 Research Focus:host-pathogen & immune response· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Kentsis· 3 shared M. Uni· 2 shared P. Cifani· 2 shared R. Koche· 2 shared S. Cheng· 2 shared A. Krivtsov· 1 shared A. N. Saito· 1 shared A. Ono· 1 shared

Activity by Year

2017-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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3 shared papersCancer Biology

A. Kentsis

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4 papers

Recent·Most cited

Epigenetic mechanisms controlling human leukemia stem cells and therapy resistance

S. Takao, V. Morell, M. Uni, A. Slavit, S. Rha, S. Cheng, L. K. Schmalbrock, F. C. Brown, S. B.- Calabuig, R. Koche, L. Velten, A. Kentsis

This study identifies a quiescent label-retaining cell population in human AML that drives disease and therapy resistance through epigenetic mechanisms.

bioRxiv · Sep 22, 2022Cancer Biology

A unique small molecule pair controls the plant circadian clock

T. N. Uehara, S. Takao, H. Matsuo, A. N. Saito, E. Ota, A. Ono, K. Itami, T. Kinoshita, J. Yamaguchi, N. Nakamichi

The paper identifies two small molecules that oppositely regulate the Arabidopsis circadian clock by altering period length, revealing their mode of action through genetic mutants.

bioRxiv · May 25, 2020 · PreprintPlant Biology

Convergent organization of aberrant MYB complex controls oncogenic gene expression in acute myeloid leukemia

S. Takao, L. Forbes, M. Uni, S. Cheng, J. M. B. Pineda, Y. Tarumoto, P. Cifani, G. Minuesa, C. Chen, M. G. Kharas, R. K. Bradley, C. R. Vakoc, R. P. Koche, A. Kentsis

This study identifies aberrant MYB complex assembly as a driver of oncogenic gene expression in AML and shows that targeting this complex can induce differentiation and apoptosis.

bioRxiv · May 5, 2020Cancer Biology

MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

F. Brown, E. Still, P. Cifani, S. Takao, C. Reed, S. Ficarro, R. Koche, P. Romanienko, W. Mark, C. O'Donnell, B. Spitzer, C. Stutzke, A. Krivtsov, G. Pouliot, J. Marto, , A. Kentsis

This study identifies MEF2C phosphorylation as a marker of chemotherapy resistance in AML and shows that inhibiting this phosphorylation can overcome resistance in MEF2C-activated cells.

bioRxiv · Feb 9, 2017Cancer Biology