ArticleIn vitro cellular & developmental biology. Animal1994
A novel pathway for retinoic acid-induced differentiation of F9 cells that is distinct from receptor-mediated trans-activation.
Article in In vitro cellular & developmental biology. Animal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 16 citations in OpenAlex.
- Biocompatible Gold Nanoparticles Ameliorate Retinoic Acid-Induced Cell Death and Induce Differentiation in F9 Teratocarcinoma Stem Cells.Nanomaterials (Basel, Switzerland) · 2018Article
- JDP2, a repressor of AP-1, recruits a histone deacetylase 3 complex to inhibit the retinoic acid-induced differentiation of F9 cells.Molecular and cellular biology · 2002Article
- p300 and ATF-2 are components of the DRF complex, which regulates retinoic acid- and E1A-mediated transcription of the c-jun gene in F9 cells.Genes & development · 1998Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoic acid (RA) has striking effects on vertebrate development and induces differentiation of several lines of cells including embryonal carcinoma F9 cells. It is generally accepted that the actions of RA are mediated by nuclear receptors for RA. However, we now provide evidence that F9 cells can differentiate in response to RA without trans-activation by nuclear receptors. Irreversible differentiation of F9 cells was induced by 18 h of exposure to RA with subsequent incubation in the absence of RA. This induction of differentiation was not blocked after inhibition of protein synthesis and mRNA synthesis during the 18-h treatment with RA, but the endogenous RA receptors failed to activate transcription from their target genes that contain the receptor-binding sequences. During the commitment to RA-induced differentiation, at least five sets of four phosphorylated proteins underwent changes in the absence of protein synthesis de novo. These results suggest that there is a novel pathway for the action of RA that is independent of nuclear receptor-mediated trans-activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.