ArticleCell communication and signaling : CCS2019
Genomic and non-genomic pathways are both crucial for peak induction of neurite outgrowth by retinoids.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Synthetic Retinoids for the Modulation of Genomic and Nongenomic Processes in Neurodegenerative Diseases.ACS omega · 2025Article
- A Comparative Study of a Potent CNS-Permeable RARβ-Modulator, Ellorarxine, in Neurons, Glia and Microglia Cells In Vitro.International journal of molecular sciences · 2025Article
- Quantitative phosphoproteomics reveals that nestin is a downstream target of dual leucine zipper kinase during retinoic acid-induced neuronal differentiation of Neuro-2a cells.BMC molecular and cell biology · 2025Article
- Editorial: The role of retinoic acid signaling in maintenance and regeneration of the CNS: from mechanisms to therapeutic targeting.Frontiers in molecular neuroscience · 2024Article
- Non-canonical retinoid signaling in neural development, regeneration and synaptic function.Frontiers in molecular neuroscience · 2024Review
- NR1D1 Stimulates Antitumor Immune Responses in Breast Cancer by Activating cGAS-STING Signaling.Cancer research · 2023Article
- The role of primed and non-primed MSC-derived conditioned media in neuroregeneration.Frontiers in molecular neuroscience · 2023Article
- Context-Dependent Role of miR-124 in Retinoic Acid-Induced Growth Cone Attraction of Regenerating Motorneurons.Cellular and molecular neurobiology · 2022Article
- All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal.Life science alliance · 2022Article
- Synthetic Diphenylacetylene-Based Retinoids Induce DNA Damage in Chinese Hamster Ovary Cells without Altering Viability.Molecules (Basel, Switzerland) · 2022Article
- Therapeutic insights elaborating the potential of retinoids in Alzheimer's disease.Frontiers in pharmacology · 2022Review
- Prox1 inhibits neurite outgrowth during central nervous system development.Cellular and molecular life sciences : CMLS · 2021Article
- Structure-functional relationship of cellular retinoic acid-binding proteins I and II interacting with natural and synthetic ligands.Acta crystallographica. Section D, Structural biology · 2021Article
- Retinoid signaling in skeletal development: Scoping the system for predictive toxicology.Reproductive toxicology (Elmsford, N.Y.) · 2021Review
- A ligand-independent fast function of RARα promotes exit from metabolic quiescence upon T cell activation and controls T cell differentiation.Mucosal immunology · 2021Article
- Decay in Retinoic Acid Signaling in Varied Models of Alzheimer's Disease and In-Vitro Test of Novel Retinoic Acid Receptor Ligands (RAR-Ms) to Regulate Protective Genes.Journal of Alzheimer's disease : JAD · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Retinoic acid (RA) is the active metabolite of vitamin A and essential for many physiological processes, particularly the induction of cell differentiation. In addition to regulating genomic transcriptional activity via RA receptors (RARs) and retinoid X receptors (RXRs), non-genomic mechanisms of RA have been described, including the regulation of ERK1/2 kinase phosphorylation, but are poorly characterised. In this study, we test the hypothesis that genomic and non-genomic mechanisms of RA are regulated independently with respect to the involvement of ligand-dependent RA receptors. A panel of 28 retinoids (compounds with vitamin A-like activity) showed a marked disparity in genomic (gene expression) versus non-genomic (ERK1/2 phosphorylation) assays. These results demonstrate that the capacity of a compound to activate gene transcription does not necessarily correlate with its ability to regulate a non-genomic activity such as ERK 1/2 phosphorylation. Furthermore, a neurite outgrowth assay indicated that retinoids that could only induce either genomic, or non-genomic activities, were not strong promoters of neurite outgrowth, and that activities with respect to both transcriptional regulation and ERK1/2 phosphorylation produced maximum neurite outgrowth. These results suggest that the development of effective retinoids for clinical use will depend on the selection of compounds which have maximal activity in non-genomic as well as genomic assays.
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Registered trials
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