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THAP1: Role in Mouse Embryonic Stem Cell Survival and Differentiation
Umeå University, Faculty of Medicine, Department of Medical Biosciences. Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
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2017 (English)In: Stem Cell Reports, ISSN 2213-6711, Vol. 9, no 1, 92-107 p.Article in journal (Refereed) Published
Abstract [en]

THAP1 (THAP [Thanatos-associated protein] domain-containing, apoptosis-associated protein 1) is a ubiquitously expressed member of a family of transcription factors with highly conserved DNA-binding and protein-interacting regions. Mutations in THAP1 cause dystonia, DYT6, a neurologic movement disorder. THAP1 downstream targets and the mechanism via which it causes dystonia are largely unknown. Here, we show that wild-type THAP1 regulates embryonic stem cell (ESC) potential, survival, and proliferation. Our findings identify THAP1 as an essential factor underlying mouse ESC survival and to some extent, differentiation, particularly neuroectodermal. Loss of THAP1 or replacement with a disease-causing mutation results in an enhanced rate of cell death, prolongs Nanog, Prdm14, and/or Rex1 expression upon differentiation, and results in failure to upregulate ectodermal genes. ChIP-Seq reveals that these activities are likely due in part to indirect regulation of gene expression.

Place, publisher, year, edition, pages
CELL PRESS , 2017. Vol. 9, no 1, 92-107 p.
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy) Developmental Biology Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:umu:diva-137943DOI: 10.1016/j.stemcr.2017.04.032ISI: 000405178400011OAI: oai:DiVA.org:umu-137943DiVA: diva2:1129427
Available from: 2017-08-03 Created: 2017-08-03 Last updated: 2017-08-03Bibliographically approved

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