Publisher Correction: Tracing the transitions from pluripotency to germ cell fate with CRISPR screening
- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
2041-1723
- Extent
-
Online-Ressource
- Language
-
Englisch
- Notes
-
online resource.
- Bibliographic citation
-
Publisher Correction: Tracing the transitions from pluripotency to germ cell fate with CRISPR screening ; volume:9 ; number:1 ; day:11 ; month:12 ; year:2018 ; pages:1 ; date:12.2018
Nature Communications ; 9, Heft 1 (11.12.2018), 1, 12.2018
- Classification
-
Biowissenschaften, Biologie
- Creator
-
Hackett, Jamie A.
Huang, Yun
Günesdogan, Ufuk
Gretarsson, Kristjan A.
Kobayashi, Toshihiro
Surani, M. Azim
- Contributor
-
SpringerLink (Online service)
- DOI
-
10.1038/s41467-018-07765-y
- URN
-
urn:nbn:de:101:1-2019012801013593952405
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 11:00 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Hackett, Jamie A.
- Huang, Yun
- Günesdogan, Ufuk
- Gretarsson, Kristjan A.
- Kobayashi, Toshihiro
- Surani, M. Azim
- SpringerLink (Online service)
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Publisher Correction: Utf1 contributes to intergenerational epigenetic inheritance of pluripotency
Metabolic regulation of pluripotency and germ cell fate through α‐ketoglutarate
Modeling signaling‐dependent pluripotency with Boolean logic to predict cell fate transitions
The proteasome complex and the maintenance of pluripotency: sustain the fate by mopping up?
Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation
Membrane potential drives the exit from pluripotency and cell fate commitment via calcium and mTOR
Chondrocyte cell fate tracing in a murine model of articular cartilage regeneration
Tracing the specificity of CRISPR-Cas nucleases in clinically relevant human cells
Genetic tool for fate mapping of Oct4 (Pou5f1)-expressing cells and their progeny past the pluripotency stage
bHLH transcription factor Math6 antagonizes TGF-\(\beta\) signalling in reprogramming, pluripotency and early cell fate decisions
Tracing the transitions from pluripotency to germ cell fate with CRISPR screening
Switching Human Cell Fate: Reprogramming via pluripotency to adipogenesis
Publisher Correction: Utf1 contributes to intergenerational epigenetic inheritance of pluripotency
Metabolic regulation of pluripotency and germ cell fate through α‐ketoglutarate
Modeling signaling‐dependent pluripotency with Boolean logic to predict cell fate transitions
The proteasome complex and the maintenance of pluripotency: sustain the fate by mopping up?
Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation
Membrane potential drives the exit from pluripotency and cell fate commitment via calcium and mTOR
Chondrocyte cell fate tracing in a murine model of articular cartilage regeneration
Tracing the specificity of CRISPR-Cas nucleases in clinically relevant human cells
Genetic tool for fate mapping of Oct4 (Pou5f1)-expressing cells and their progeny past the pluripotency stage
bHLH transcription factor Math6 antagonizes TGF-\(\beta\) signalling in reprogramming, pluripotency and early cell fate decisions
Tracing the transitions from pluripotency to germ cell fate with CRISPR screening
Switching Human Cell Fate: Reprogramming via pluripotency to adipogenesis
Publisher Correction: Utf1 contributes to intergenerational epigenetic inheritance of pluripotency
Metabolic regulation of pluripotency and germ cell fate through α‐ketoglutarate
Modeling signaling‐dependent pluripotency with Boolean logic to predict cell fate transitions
The proteasome complex and the maintenance of pluripotency: sustain the fate by mopping up?
Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation
Membrane potential drives the exit from pluripotency and cell fate commitment via calcium and mTOR
Chondrocyte cell fate tracing in a murine model of articular cartilage regeneration
Tracing the specificity of CRISPR-Cas nucleases in clinically relevant human cells
Genetic tool for fate mapping of Oct4 (Pou5f1)-expressing cells and their progeny past the pluripotency stage