Dichotomous role of Shp2 for naïve and primed pluripotency maintenance in embryonic stem cells
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1757-6512
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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Dichotomous role of Shp2 for naïve and primed pluripotency maintenance in embryonic stem cells ; volume:13 ; number:1 ; day:18 ; month:7 ; year:2022 ; pages:1-14 ; date:12.2022
Stem cell research & therapy ; 13, Heft 1 (18.7.2022), 1-14, 12.2022
- Creator
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Kim, Seong-Min
Kwon, Eun-Ji
Kim, Yun-Jeong
Go, Young-Hyun
Oh, Ji-Young
Park, Seokwoo
Do, Jeong Tae
Kim, Keun-Tae
Cha, Hyuk-Jin
- Contributor
-
SpringerLink (Online service)
- DOI
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10.1186/s13287-022-02976-z
- URN
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urn:nbn:de:101:1-2022092722530585925477
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
15.08.2025, 7:24 AM CEST
Data provider
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Kim, Seong-Min
- Kwon, Eun-Ji
- Kim, Yun-Jeong
- Go, Young-Hyun
- Oh, Ji-Young
- Park, Seokwoo
- Do, Jeong Tae
- Kim, Keun-Tae
- Cha, Hyuk-Jin
- SpringerLink (Online service)
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Comparative analysis of naive, primed and ground state pluripotency in mouse embryonic stem cells originating from the same genetic background
Discordance between chromatin accessibility and transcriptional activity during the human primed-to-naïve pluripotency transition process
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 stepwise mode of TGFβ-SMAD signaling and DNA methylation regulates naïve-to-primed pluripotency and differentiation
Chromatin landscape dynamics during reprogramming towards human naïve and primed pluripotency reveals the divergent function of PRDM1 isoforms
TET activity safeguards pluripotency throughout embryonic dormancy
Taking the RISC of exiting naïve pluripotency
A non-canonical BRD9-containing BAF chromatin remodeling complex regulates naive pluripotency in mouse embryonic stem cells
Epigenetic differences between naïve and primed pluripotent stem cells
Cpt1a Drives primed-to-naïve pluripotency transition through lipid remodeling
The metabolic network model of primed/naive human embryonic stem cells underlines the importance of oxidation-reduction potential and tryptophan metabolism in primed pluripotency
Comparative analysis of naive, primed and ground state pluripotency in mouse embryonic stem cells originating from the same genetic background
Discordance between chromatin accessibility and transcriptional activity during the human primed-to-naïve pluripotency transition process
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 stepwise mode of TGFβ-SMAD signaling and DNA methylation regulates naïve-to-primed pluripotency and differentiation
Chromatin landscape dynamics during reprogramming towards human naïve and primed pluripotency reveals the divergent function of PRDM1 isoforms
TET activity safeguards pluripotency throughout embryonic dormancy
Taking the RISC of exiting naïve pluripotency
A non-canonical BRD9-containing BAF chromatin remodeling complex regulates naive pluripotency in mouse embryonic stem cells
Epigenetic differences between naïve and primed pluripotent stem cells
Cpt1a Drives primed-to-naïve pluripotency transition through lipid remodeling
The metabolic network model of primed/naive human embryonic stem cells underlines the importance of oxidation-reduction potential and tryptophan metabolism in primed pluripotency
Comparative analysis of naive, primed and ground state pluripotency in mouse embryonic stem cells originating from the same genetic background
Discordance between chromatin accessibility and transcriptional activity during the human primed-to-naïve pluripotency transition process
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 stepwise mode of TGFβ-SMAD signaling and DNA methylation regulates naïve-to-primed pluripotency and differentiation
Chromatin landscape dynamics during reprogramming towards human naïve and primed pluripotency reveals the divergent function of PRDM1 isoforms
TET activity safeguards pluripotency throughout embryonic dormancy
Taking the RISC of exiting naïve pluripotency
A non-canonical BRD9-containing BAF chromatin remodeling complex regulates naive pluripotency in mouse embryonic stem cells