Author

Hajime Okada

National Institute of GeneticsORCID 0000-0002-3204-3633Unclaimed ORCID profile · follow to get notified of new preprints

Additional preprints under this name without ORCID

Hajime Okada1 paper · Tel Aviv University

Biology Disciplines

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Developmental Biology· 1 Genetics· 1 Molecular Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Approach:statistical model· 1

Frequent Co-Authors

Yumiko SagaiD· 2 shared Atsushi MiyajimaiD· 1 shared Atsushi ToyodaiD· 1 shared Hiroshi MoriiD· 1 shared Jessica KimiD· 1 shared Masafumi MuraokaiD· 1 shared Masatsugu EmaiD· 1 shared Minami YamadaiD· 1 shared

Activity by Year

2022-2022 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersGenetics

Yumiko SagaORCID

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3 papers

Recent·Most cited

The RNA helicase DDX6 controls early mouse embryogenesis by repressing aberrant inhibition of BMP signaling through miRNA-mediated gene silencing

Jessica Kim, Masafumi Muraoka, Rieko Ajima, Hajime Okada, Atsushi Toyoda, Hiroshi Mori, Yumiko Saga

This study shows DDX6 regulates early mouse embryogenesis by repressing negative BMP regulators via miRNA-mediated gene silencing, affecting cell lineage specification and germ layer development.

PLoS Genetics · Oct 5, 2022Peer-reviewedGenetics

KLF5-regulated extracellular matrix remodeling secures biliary epithelial tissue integrity against cholestatic liver injury

Minami Yamada, Hajime Okada, Masatsugu Ema, Yamato Kikkawa, Atsushi Miyajima, Tohru Itoh

This study identifies KLF5's role in maintaining biliary epithelial integrity during cholestatic injury by regulating extracellular matrix remodeling and cell adhesion.

bioRxiv · Jan 25, 2022 · PreprintDevelopmental Biology

Repurposing of the enhancer-promoter communication underlies the compensation of Mesp2 by Mesp1

Hajime Okada, Yumiko Saga

The paper identifies a novel genetic compensation mechanism where the Mesp2 enhancer interacts with the Mesp1 promoter to upregulate Mesp1 in response to Mesp2 loss.

PLoS Genetics · Jan 13, 2022Peer-reviewedMolecular Biology