Author

Y. Obata

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· 2 Bioengineering· 1 Cell Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 5 Organism:human· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Assay:proteomics· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell-cell communication· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

I. Shiina· 3 shared R. Abe· 3 shared T. Nishida· 3 shared M. Natsume· 2 shared M. Niwa· 2 shared M. Shimonaka· 2 shared T. Murata· 2 shared A. A. Crofts· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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Curved chords = mutual co-authorship

3 shared papersCancer Biology

I. Shiina

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Brefeldin A and M-COPA block the export of RTKs from the endoplasmic reticulum via simultaneous inactivation of ARF1, ARF4, and ARF5

M. Natsume, M. Niwa, S. Ichikawa, T. Okamoto, H. Tsutsui, D. Usukura, T. Murata, R. Abe, M. Shimonaka, T. Nishida, I. Shiina, Y. Obata

This study shows that BFA and M-COPA inhibit RTK export from the ER by inactivating ARF1, ARF4, and ARF5, leading to cancer cell apoptosis.

bioRxiv · Oct 11, 2023Cell Biology

Whole-bone toughness is linked to canal and osteocyte lacunae deficits in the ZDSD type 2 diabetic rat model

W. J. Woolley, Y. Obata, K. Martin, C. Acevedo

This study links reduced bone toughness in T2DM rats to microstructural changes in canals and osteocyte lacunae, along with AGEs accumulation.

bioRxiv · Mar 7, 2023 · PreprintBioengineering

Golgi retention and oncogenic KIT signaling via PLCγ2-PKD2-PI4KIIIβ activation in GIST cells

Y. Obata, K. Kurokawa, T. Tojima, M. Natsume, I. Shiina, T. Takahashi, R. Abe, A. Nakano, T. Nishida

This study identifies the molecular mechanisms by which mutant KIT remains in the Golgi and activates oncogenic signaling in GIST cells.

bioRxiv · Dec 19, 2022 · PreprintCancer Biology

Macrophages regulate gastrointestinal motility through complement component 1q

M. Pendse, Y. Li, C. N. Salinas, G. Quinn, N. Vo, D. C. Propheter, C. Dende, A. A. Crofts, E. Koo, B. Hassell, K. A. Ruhn, P. Raj, Y. Obata, L. V. Hooper

This study identifies complement component 1q (C1q) as a macrophage-derived factor that regulates gastrointestinal motility by interacting with the enteric nervous system.

bioRxiv · Jan 27, 2022Immunology

FLT3-ITD transduces autonomous growth signals during its biosynthetic trafficking in acute myelogenous leukemia cells.

K. Yamawaki, I. Shiina, T. Murata, S. Tateyama, Y. Maekawa, M. Niwa, M. Shimonaka, K. Okamoto, T. Suzuki, T. Nishida, R. Abe, Y. Obata

This study shows FLT3-ITD accumulates in the Golgi apparatus in AML cells, activates signaling pathways like STAT5 and AKT/ERK during biosynthetic trafficking, and its tyrosine kinase activity is required for this retention.

bioRxiv · Jan 1, 2021 · PreprintCancer Biology