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AKT1 induces Nanog promoter in a SUMOylation-dependent manner in different pluripotent contexts
AKT/PKB is a kinase crucial for pluripotency maintenance in pluripotent stem cells. Multiple post-translational modifications modulate its activity. We have previously demonstrated that AKT1 induces the expression of the pluripotency transcription factor Nanog in a SUMOylation-dependent manner in mo...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10623886/ https://www.ncbi.nlm.nih.gov/pubmed/37919788 http://dx.doi.org/10.1186/s13104-023-06598-3 |
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author | Francia, Marcos Gabriel Verneri, Paula Oses, Camila Vazquez Echegaray, Camila Garcia, Mora Reneé Toro, Ayelen Levi, Valeria Guberman, Alejandra Sonia |
author_facet | Francia, Marcos Gabriel Verneri, Paula Oses, Camila Vazquez Echegaray, Camila Garcia, Mora Reneé Toro, Ayelen Levi, Valeria Guberman, Alejandra Sonia |
author_sort | Francia, Marcos Gabriel |
collection | PubMed |
description | AKT/PKB is a kinase crucial for pluripotency maintenance in pluripotent stem cells. Multiple post-translational modifications modulate its activity. We have previously demonstrated that AKT1 induces the expression of the pluripotency transcription factor Nanog in a SUMOylation-dependent manner in mouse embryonic stem cells. Here, we studied different cellular contexts and main candidates that could mediate this induction. Our results strongly suggest the pluripotency transcription factors OCT4 and SOX2 are not essential mediators. Additionally, we concluded that this induction takes place in different pluripotent contexts but not in terminally differentiated cells. Finally, the cross-matching analysis of ESCs, iPSCs and MEFs transcriptomes and AKT1 phosphorylation targets provided new clues about possible factors that could be involved in the SUMOylation-dependent Nanog induction by AKT. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-023-06598-3. |
format | Online Article Text |
id | pubmed-10623886 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-106238862023-11-04 AKT1 induces Nanog promoter in a SUMOylation-dependent manner in different pluripotent contexts Francia, Marcos Gabriel Verneri, Paula Oses, Camila Vazquez Echegaray, Camila Garcia, Mora Reneé Toro, Ayelen Levi, Valeria Guberman, Alejandra Sonia BMC Res Notes Research Note AKT/PKB is a kinase crucial for pluripotency maintenance in pluripotent stem cells. Multiple post-translational modifications modulate its activity. We have previously demonstrated that AKT1 induces the expression of the pluripotency transcription factor Nanog in a SUMOylation-dependent manner in mouse embryonic stem cells. Here, we studied different cellular contexts and main candidates that could mediate this induction. Our results strongly suggest the pluripotency transcription factors OCT4 and SOX2 are not essential mediators. Additionally, we concluded that this induction takes place in different pluripotent contexts but not in terminally differentiated cells. Finally, the cross-matching analysis of ESCs, iPSCs and MEFs transcriptomes and AKT1 phosphorylation targets provided new clues about possible factors that could be involved in the SUMOylation-dependent Nanog induction by AKT. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-023-06598-3. BioMed Central 2023-11-03 /pmc/articles/PMC10623886/ /pubmed/37919788 http://dx.doi.org/10.1186/s13104-023-06598-3 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Note Francia, Marcos Gabriel Verneri, Paula Oses, Camila Vazquez Echegaray, Camila Garcia, Mora Reneé Toro, Ayelen Levi, Valeria Guberman, Alejandra Sonia AKT1 induces Nanog promoter in a SUMOylation-dependent manner in different pluripotent contexts |
title | AKT1 induces Nanog promoter in a SUMOylation-dependent manner in different pluripotent contexts |
title_full | AKT1 induces Nanog promoter in a SUMOylation-dependent manner in different pluripotent contexts |
title_fullStr | AKT1 induces Nanog promoter in a SUMOylation-dependent manner in different pluripotent contexts |
title_full_unstemmed | AKT1 induces Nanog promoter in a SUMOylation-dependent manner in different pluripotent contexts |
title_short | AKT1 induces Nanog promoter in a SUMOylation-dependent manner in different pluripotent contexts |
title_sort | akt1 induces nanog promoter in a sumoylation-dependent manner in different pluripotent contexts |
topic | Research Note |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10623886/ https://www.ncbi.nlm.nih.gov/pubmed/37919788 http://dx.doi.org/10.1186/s13104-023-06598-3 |
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