Nac1 facilitates pluripotency gene activation for establishing somatic cell reprogramming
Transcription factors play a central role in pluripotency transcription circuitry for establishing pluripotent reprogramming. Master transcription factors Oct4, Nanog, and Sox2 are known to form the core of the pluripotency transcription network. Other transcription factors also play critical roles...
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| Published in: | Biochemical and biophysical research communications Vol. 518; no. 2; pp. 253 - 258 |
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| Main Authors: | , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
United States
Elsevier Inc
15.10.2019
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| Subjects: | |
| ISSN: | 0006-291X, 1090-2104, 1090-2104 |
| Online Access: | Get full text |
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| Summary: | Transcription factors play a central role in pluripotency transcription circuitry for establishing pluripotent reprogramming. Master transcription factors Oct4, Nanog, and Sox2 are known to form the core of the pluripotency transcription network. Other transcription factors also play critical roles for further refining the core circuitry for pluripotency in induced pluripotent stem (iPS) cells. Here, we reported that Nac1 interacted with the master pluripotent factors Oct4 and Nanog co-occupies gene promoters bound by these transcriptional factors for establishing pluripotency. Moreover, this interaction coordinates gene expression with H3K4me3 in the somatic cell reprogramming. Knockdown of Nac1 suppressed somatic cell reprogramming, whereas overexpression of Nac1 resulted in enhanced efficiency of induced pluripotent cell generation. Altogether, these results reveal the genome wide role for Nac1 in the contribution to the pluripotency circuitry and the regulation of the establishing pluripotent state.
•Nac1 co-occupies gene promoters bound by Oct4 and Nanog for establishing pluripotency.•Nac1 coordinates gene expression with H3K4me3 in the somatic cell reprogramming.•Nac1 contribute to the pluripotency circuitry and the establishing pluripotent state. |
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| Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| ISSN: | 0006-291X 1090-2104 1090-2104 |
| DOI: | 10.1016/j.bbrc.2019.08.043 |