Author

Michael Barber

Wellcome/MRC Cambridge Stem Cell InstitutePrimary ORCID profile (0000-0002-2673-1210 · 2 papers)Unclaimed ORCID profile · follow to get notified of new preprints

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Michael BarberiD2 papers · Institute of Genetics and Cancer

Biology Disciplines

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Developmental Biology· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Research Focus:gene regulatory network inference· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Assay:DNA methylation· 1

Frequent Co-Authors

Masaki KinoshitaiD· 3 shared Sabine DietmanniD· 3 shared Austin G SmithiD· 2 shared William M. MansfieldiD· 2 shared Brian HendrichiD· 1 shared Daniel Spindlow· 1 shared Giuliano Giuseppe StirparoiD· 1 shared Jennifer NicholsiD· 1 shared

Activity by Year

2019-2021 · peak 1/yr

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10 top collaborators · 30 mutual co-author links

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3 shared papersDevelopmental Biology

Masaki KinoshitaORCID

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3 papers

Recent·Most cited

Disabling de novo DNA methylation in embryonic stem cells allows an illegitimate fate trajectory

Masaki Kinoshita, Meng Amy Li, Michael Barber, William M. Mansfield, Sabine Dietmann, Austin G Smith

The paper shows that disabling de novo DNA methylation in embryonic stem cells causes them to adopt a trophoblast fate instead of proper differentiation, due to misexpression of Ascl2.

Proceedings of the National Academy of Sciences · Sep 13, 2021Peer-reviewedDevelopmental Biology

Capture of mouse and human stem cells with features of formative pluripotency

Masaki Kinoshita, Michael Barber, William M. Mansfield, Yingzhi Cui, Daniel Spindlow, Giuliano Giuseppe Stirparo, Sabine Dietmann, Jennifer Nichols, Austin G Smith

The paper identifies and characterizes formative stem cells in mice and humans, showing they have unique transcriptional and epigenetic features compared to naive and primed pluripotent cells.

Cell stem cell · Dec 2, 2020Peer-reviewedDevelopmental Biology

Subunit redundancy within the NuRD complex ensures fidelity of ES cell lineage commitment

Thomas Burgold, Michael Barber, Susan L. Kloet, Julie Cramard, Sarah Gharbi, Robin Floyd, Masaki Kinoshita, Meryem Ralser, Michiel Vermeulen, Nicola Reynolds, Sabine Dietmann, Brian Hendrich

The paper shows that MTA proteins in ES cell NuRD complex are functionally redundant, and NuRD is essential for maintaining differentiation trajectory during early lineage commitment.

The EMBO Journal · Apr 29, 2019Peer-reviewedDevelopmental Biology