Author

Eishou Matsuda

Nara Institute of Science and TechnologyORCID 0000-0002-8008-4552Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cell Biology· 1 Developmental Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1

Frequent Co-Authors

Yasumasa IshidaiD· 2 shared Chio OkaiD· 1 shared Hiroyuki Nagaoka· 1 shared Miki Nishio· 1 shared Noriaki SasaiiD· 1 shared Nunuk Aries NurulitaiD· 1 shared Shiomi Ohta· 1 shared Shogo Tada· 1 shared

Activity by Year

2021-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersCell Biology

Yasumasa IshidaORCID

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2 papers

Recent·Most cited

Zbtb38 transcriptionally activates XIAP to regulate apoptosis in development and cancer

Toshiaki Shigeoka, Hiroyuki Nagaoka, Nunuk Aries Nurulita, Shogo Tada, Yasumasa Bessho, Yasumasa Ishida, Eishou Matsuda

This study identifies Zbtb38 as a transcriptional activator of XIAP, showing its role in regulating apoptosis during development and cancer, with implications for therapeutic targeting.

Journal of Molecular Cell Biology · Jan 1, 2026Peer-reviewedCell Biology

Heterozygous loss of ZBTB38 leads to early embryonic lethality in mice via suppressing Nanog and Sox2

Miki Nishio, Takuya Matsuura, Shunya Hibi, Shiomi Ohta, Chio Oka, Noriaki Sasai, Yasumasa Ishida, Eishou Matsuda

This study shows that heterozygous ZBTB38 loss in mice causes early embryonic lethality by reducing Nanog and Sox2 expression, while ZBTB38 is not essential for ES cell establishment.

bioRxiv · Aug 19, 2021 · PreprintDevelopmental Biology