The DOI matches its Crossref record; 269 of the 269 references it cites were found in a registry or an index.
Retinoic acid signaling and neuronal differentiation
Open accessAbstract
The identification of neurological symptoms caused by vitamin A deficiency pointed to a critical, early developmental role of vitamin A and its metabolite, retinoic acid (RA). The ability of RA to induce post-mitotic, neural phenotypes in various stem cells, in vitro, served as early evidence that RA is involved in the switch between proliferation and differentiation. In vivo studies have expanded this "opposing signal" model, and the number of primary neurons an embryo develops is now known to depend critically on the levels and spatial distribution of RA. The proneural and neurogenic transcription factors that control the exit of neural progenitors from the cell cycle and allow primary neurons to develop are partly elucidated, but the downstream effectors of RA receptor (RAR) signaling (many of which are putative cell cycle regulators) remain largely unidentified. The molecular mechanisms underlying RA-induced primary neurogenesis in anamniote embryos are starting to be revealed; however, these data have been not been extended to amniote embryos. There is growing evidence that bona fide RARs are found in some mollusks and other invertebrates, but little is known about their necessity or functions in neurogenesis. One normal function of RA is to regulate the cell cycle to halt proliferation, and loss of RA signaling is associated with dedifferentiation and the development of cancer. Identifying the genes and pathways that mediate cell cycle exit downstream of RA will be critical for our understanding of how to target tumor differentiation. Overall, elucidating the molecular details of RAR-regulated neurogenesis will be decisive for developing and understanding neural proliferation-differentiation switches throughout development.
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“Initial studies have used RA as a potent regulator of neural differentiation72.”
From Advances and challenges in retinoid delivery systems in regenerative and therapeutic medicine (2020) · cites this paper as [72]
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Allosteric Regulation in the Ligand Binding Domain of Retinoic Acid Receptorγ
Chebaro, Y., Sirigu, S., Amal, I., Lutzing, R., Stote, R. H., Rochette-Egly, C., Rochel, N., & Dejaegere, A. (2017) · PLOS ONE · doi:10.1371/journal.pone.0171043 · Cited by 8
Metadata
- Authors
- Janesick, A., Wu, S. C., & Blumberg, B.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- Blumberg, Bruce
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2015-01-06
- Volume
- 72
- Issue
- 8
- Pages
- 1559-1576
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11113123
- OpenAlex
- W2117145998
- Cited by
- 295
- References
- 268
- Citations by year
- 2026: 15 · 2025: 37 · 2024: 30 · 2023: 36 · 2022: 25 · 2021: 44 · 2020: 31 · 2019: 24 · 2018: 22 · 2017: 16 · 2016: 13 · 2015: 2
- FWCI
- 2.22
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
- Funders
- National Science Foundation
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- retinoic acid signaling, neuronal differentiation, primary neurogenesis, retinoic acid receptor, proneural transcription factors, vitamin A deficiency, dedifferentiation, tumor differentiation
- MeSH terms
- Animals, Antigens, Neoplasm, Antineoplastic Agents, Humans, Neoplasms, Neurons, Tretinoin, Signal Transduction, Receptors, Retinoic Acid, Cell Cycle Proteins, Neurogenesis
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