ArticleThe Journal of biological chemistry2012
Retinoic acid induces neurogenesis by activating both retinoic acid receptors (RARs) and peroxisome proliferator-activated receptor β/δ (PPARβ/δ).
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed.
- Peroxisome Proliferator-Activated Receptor Delta (PPARδ) as a Metabolic Gatekeeper of Cerebrovascular Integrity.Journal of molecular neuroscience : MN · 2026Review
- Vitamin A supplementation restores neuroanatomical integrity and behavior in a valproic acid-induced autism model.Journal of molecular histology · 2025Article
- Protective Effect of FABP5 Against 6-OHDA Induced Parkinson's Disease Via PPARγ/SIRT1/PGC-1α Signaling Pathway.Neurochemical research · 2025Article
- Meningeal-derived retinoic acid regulates neurogenesis via suppression of Notch and Sox2.Cell reports · 2025Article
- Article
- 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
- A Missense Variant inGenes · 2024Article
- Identification of MicroRNA Profiles in Fetal Spina Bifida: The Role in Pathomechanism and Diagnostic Significance.International journal of molecular sciences · 2024Article
- The Contribution of Hippocampal All-Trans Retinoic Acid (ATRA) Deficiency to Alzheimer's Disease: A Narrative Overview of ATRA-Dependent Gene Expression in Post-Mortem Hippocampal Tissue.Antioxidants (Basel, Switzerland) · 2023Review
- Vitamin A injection at birth improves muscle growth in lambs.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
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- Centella asiatica (L.) Urban. Attenuates Cell Damage in Hydrogen Peroxide-Induced Oxidative Stress in Transgenic Murine Embryonic Stem Cell Line-Derived Neural-Like Cells: A Preliminary Study for Potential Treatment of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- The covalent reactivity of functionalized 5-hydroxy-butyrolactams is the basis for targeting of fatty acid binding protein 5 (FABP5) by the neurotrophic agent MT-21.RSC chemical biology · 2022Article
- DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022Review
- Article
- The Biological Functions and Regulatory Mechanisms of Fatty Acid Binding Protein 5 in Various Diseases.Frontiers in cell and developmental biology · 2022Review
- The Dynamic Proteome of Oligodendrocyte Lineage Differentiation Features Planar Cell Polarity and Macroautophagy Pathways.GigaScience · 2020Article
- Deletion of theInternational journal of molecular sciences · 2020Article
- Conversion of human urine-derived cells into neuron-like cells by small molecules.Molecular biology reports · 2020Article
- Peptide Regulation of Cell Differentiation.Stem cell reviews and reports · 2020Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors.
Funding
Abstract
Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) β/δ and their respective cognate lipid-binding proteins CRABP-II and FABP5. RA induces neuronal differentiation, but the contributions of the two transcriptional pathways of the hormone to the process are unknown. Here, we show that the RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARβ/δ path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. In contrast with its inhibitory activity in the early steps of neurogenesis, the FABP5/PPARβ/δ path promotes differentiation of neuronal progenitors to mature neurons, an activity mediated in part by the PPARβ/δ target gene PDK1. Hence, RA-induced neuronal differentiation is mediated through RAR in the early stages and through PPARβ/δ in the late stages of the process. The switch in RA signaling is accomplished by a transient up-regulation of RARβ concomitantly with a transient increase in the CRABP-II/FABP5 ratio at early stages of differentiation. In accordance with these conclusions, hippocampi of FABP5-null mice display excess accumulation of neuronal progenitor cells and a deficit in mature neurons versus wild-type animals.
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