ArticleStem cell reports2023
Retention of ERK in the cytoplasm mediates the pluripotency of embryonic stem cells.
Article in Stem cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Thrombospondin 1-CD47 Signalling Modulates Vascular Smooth Muscle Cell Senescence in Chronic Kidney Disease.International journal of molecular sciences · 2026Article
- Mitochondrial gatekeeper in hepatocellular carcinoma: Unraveling the multifaceted roles of VDAC in metabolic reprogramming, apoptosis evasion and therapeutic innovation (Review).Molecular medicine reports · 2026Review
- Importin-7 promotes tension-induced osteogenesis by regulating RUNX2 nuclear translocation during orthodontic tooth movement.Scientific reports · 2025Article
- ERK2 Is a Promoter of Cancer Cell Growth and Migration in Colon Adenocarcinoma.Antioxidants (Basel, Switzerland) · 2024Article
- A Simplified and Effective Approach for the Isolation of Small Pluripotent Stem Cells Derived from Human Peripheral Blood.Biomedicines · 2023Article
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
The dynamic subcellular localization of ERK1/2 plays an important role in regulating cell fate. Differentiation of mouse embryonic stem cells (mESCs) involves inductive stimulation of ERK1/2, and therefore, inhibitors of the ERK cascade are used to maintain pluripotency. Interestingly, we found that in pluripotent mESCs, ERK1/2 do not translocate to the nucleus either before or after stimulation. This inhibition of nuclear translocation may be dependent on a lack of stimulated ERK1/2 interaction with importin7 rather than a lack of ERK1/2 phosphorylation activating translocation. At late stages of naive-to-primed transition, the action of the translocating machinery is restored, leading to elevation in ERK1/2-importin7 interaction and their nuclear translocation. Importantly, forcing ERK2 into the naive cells' nuclei accelerates their early differentiation, while prevention of the translocation restores stem cells' pluripotency. These results indicate that prevention of nuclear ERK1/2 translocation serves as a safety mechanism for keeping pluripotency of mESCs.
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Registered trials
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