Negative feedback via RSK modulates Erk‐dependent progression from naïve pluripotency
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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Online-Ressource
- Language
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Englisch
- Bibliographic citation
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Negative feedback via RSK modulates Erk‐dependent progression from naïve pluripotency ; volume:19 ; number:8 ; year:2018 ; extent:15
EMBO reports / European Molecular Biology Organization ; 19, Heft 8 (2018) (gesamt 15)
- Creator
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Nett, Isabelle RE
Mulas, Carla
Gatto, Laurent
Lilley, Kathryn S.
Smith, Austin
- DOI
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10.15252/embr.201745642
- URN
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urn:nbn:de:101:1-2022090506413322726700
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:30 AM CEST
Data provider
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Nett, Isabelle RE
- Mulas, Carla
- Gatto, Laurent
- Lilley, Kathryn S.
- Smith, Austin
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Esrrb extinction triggers dismantling of naïve pluripotency and marks commitment to differentiation
Transient upregulation of IRF1 during exit from naive pluripotency confers viral protection
Nuclear localization of mitochondrial TCA cycle enzymes modulates pluripotency via histone acetylation
Nuclear receptor-SINE B1 network modulates expanded pluripotency in blastoids and blastocysts
MTCH2-mediated mitochondrial fusion drives exit from naïve pluripotency in embryonic stem cells
Cooperative genetic networks drive embryonic stem cell transition from naïve to formative pluripotency
A defined glycosylation regulatory network modulates total glycome dynamics during pluripotency state transition
Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation
Stat3 promotes mitochondrial transcription and oxidative respiration during maintenance and induction of naive pluripotency
Taking the RISC of exiting naïve pluripotency
Epigenetic inheritance is gated by naïve pluripotency and Dppa2
Cpt1a Drives primed-to-naïve pluripotency transition through lipid remodeling
Esrrb extinction triggers dismantling of naïve pluripotency and marks commitment to differentiation
Transient upregulation of IRF1 during exit from naive pluripotency confers viral protection
Nuclear localization of mitochondrial TCA cycle enzymes modulates pluripotency via histone acetylation
Nuclear receptor-SINE B1 network modulates expanded pluripotency in blastoids and blastocysts
MTCH2-mediated mitochondrial fusion drives exit from naïve pluripotency in embryonic stem cells
Cooperative genetic networks drive embryonic stem cell transition from naïve to formative pluripotency
A defined glycosylation regulatory network modulates total glycome dynamics during pluripotency state transition
Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation
Stat3 promotes mitochondrial transcription and oxidative respiration during maintenance and induction of naive pluripotency
Taking the RISC of exiting naïve pluripotency
Epigenetic inheritance is gated by naïve pluripotency and Dppa2
Cpt1a Drives primed-to-naïve pluripotency transition through lipid remodeling
Esrrb extinction triggers dismantling of naïve pluripotency and marks commitment to differentiation
Transient upregulation of IRF1 during exit from naive pluripotency confers viral protection
Nuclear localization of mitochondrial TCA cycle enzymes modulates pluripotency via histone acetylation
Nuclear receptor-SINE B1 network modulates expanded pluripotency in blastoids and blastocysts
MTCH2-mediated mitochondrial fusion drives exit from naïve pluripotency in embryonic stem cells
Cooperative genetic networks drive embryonic stem cell transition from naïve to formative pluripotency
A defined glycosylation regulatory network modulates total glycome dynamics during pluripotency state transition
Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation