The DOI matches its Crossref record; 133 of the 133 references it cites were found in a registry or an index.
Retinoids regulate stem cell differentiation
Open accessAbstract
Retinoids are ubiquitous signaling molecules that influence nearly every cell type, exert profound effects on development, and complement cancer chemotherapeutic regimens. All‐trans retinoic acid (RA) and other active retinoids are generated from vitamin A (retinol), but key aspects of the signaling pathways required to produce active retinoids remain unclear. Retinoids generated by one cell type can affect nearby cells, so retinoids also function in intercellular communication. RA induces differentiation primarily by binding to RARs, transcription factors that associate with RXRs and bind RAREs in the nucleus. Binding of RA: (1) initiates changes in interactions of RAR/RXRs with co‐repressor and co‐activator proteins, activating transcription of primary target genes; (2) alters interactions with proteins that induce epigenetic changes; (3) induces transcription of genes encoding transcription factors and signaling proteins that further modify gene expression (e.g., FOX03A, Hoxa1, Sox9, TRAIL, UBE2D3); and (4) results in alterations in estrogen receptor α signaling. Proteins that bind at or near RAREs include Sin3a, N‐CoR1, PRAME, Trim24, NRIP1, Ajuba, Zfp423, and MN1/TEL. Interactions among retinoids, RARs/RXRs, and these proteins explain in part the powerful effects of retinoids on stem cell differentiation. Studies of this retinol signaling cascade enhance our ability to understand and regulate stem cell differentiation for therapeutic and scientific purposes. In cancer chemotherapeutic regimens retinoids can promote tumor cell differentiation and/or induce proteins that sensitize tumors to drug combinations. Mechanistic studies of retinoid signaling continue to suggest novel drug targets and will improve therapeutic strategies for cancer and other diseases, such as immune‐mediated inflammatory diseases. J. Cell. Physiol. 226: 322–330, 2011. © 2010 Wiley‐Liss, Inc.
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“Carotenoids also act as antioxidants [126,127,128,129,130,131,132].”
From Vitamin A Update: Forms, Sources, Kinetics, Detection, Function, Deficiency, Therapeutic Use and Toxicity (2021) · cites this paper as [127]
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Metadata
- Authors
- Gudas, L. J., & Wagner, J. A.
- Affiliations
- Cornell University (US)
- Corresponding author
- Gudas, Lorraine J.
- ORCID
- Gudas, Lorraine J.
- Venue
- Journal of Cellular Physiology
- Publisher
- Wiley
- Published
- 2010-11-26
- Volume
- 226
- Issue
- 2
- Pages
- 322-330
- ISSN
- 0021-9541 (ISSN-L)
- 1097-4652
- PMC
- PMC3315372
- OpenAlex
- W2108254285
- Cited by
- 395
- References
- 133
- Citations by year
- 2026: 7 · 2025: 18 · 2024: 26 · 2023: 25 · 2022: 29 · 2021: 20 · 2020: 28 · 2019: 21 · 2018: 22 · 2017: 31 · 2016: 27 · 2015: 29 · 2014: 22 · 2013: 40 · 2012: 25
- FWCI
- 2.50
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Cellular Physiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA043796)
- National Institute of Dental and Craniofacial Research (R01DE010389)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Keywords
- retinoids, all-trans retinoic acid, stem cell differentiation, retinoic acid receptor, retinoid X receptor, epigenetic regulation, drug sensitization, therapeutic target
- MeSH terms
- Animals, Cell Differentiation, Retinoids, Stem Cells, Transcription Factors, Transcription, Genetic, Tumor Cells, Cultured, Signal Transduction, beta Catenin, TNF-Related Apoptosis-Inducing Ligand
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