ArticleScientific reports2014
Tal2 expression is induced by all-trans retinoic acid in P19 cells prior to acquisition of neural fate.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 9 citations in OpenAlex.
- Retinoic acid promotes expression of inflammatory factors in proliferative adult human heart cells.American journal of physiology. Cell physiology · 2026Article
- Deletion of theInternational journal of molecular sciences · 2020Article
- Epigenetics of Skeletal Muscle-Associated Genes in theEpigenomes · 2020Article
- Reconstructed cell fate-regulatory programs in stem cells reveal hierarchies and key factors of neurogenesis.Genome research · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
TAL2 is a member of the basic helix-loop-helix family and is essential for the normal development of the mouse brain. However, the function of TAL2 during brain development is unclear. P19 cells are pluripotent mouse embryonal carcinoma cells that adopt neural fates upon exposure to all-trans retinoic acid (atRA) and culture in suspension. We found that the expression of Tal2 gene was induced in P19 cells after addition of atRA in suspension culture. Tal2 expression was detected within 3 h after the induction, and had nearly returned to basal levels by 24 h. When GFP-tagged TAL2 (GFP-TAL2) was expressed in P19 cells, we observed GFP-TAL2 in the nucleus. Moreover, we showed that atRA and retinoic acid receptor α regulated Tal2 expression. These results demonstrate for the first time that atRA induces Tal2 expression in P19 cells, and suggest that TAL2 commits to the acquisition of neural fate in brain development.
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