EMBO Retinoids 2011: Mechanisms, Biology and Pathology of Signaling by Retinoic Acid and Retinoic Acid Receptors
Open accessAbstract
Retinoic acid (RA) is one of the principal active metabolites of vitamin A (retinol) which mediates a spectrum of critical physiological and developmental processes. Transcriptional regulation by RA is mediated primarily by members of the retinoic acid receptor (RAR) subfamily of the nuclear receptor (NR) superfamily of transcription factors. NRs bind specific genomic DNA sequence motifs and engage coregulators and components of the basal transcription machinery to effect transcriptional regulation at target gene promoters. Disruption of signaling by retinoic acid is thought to underlie the etiology of a number of inflammatory and neoplastic diseases including breast cancer and haematological malignancies. A meeting of international researchers in retinoid signaling was convened in Strasbourg in September 2011 under the auspices of the European Molecular Biology Organization (EMBO). Retinoids 2011 encompassed myriad mechanistic, biological and pathological aspects of these hormones and their cognate receptors, as well as setting these advances in the context of wider current questions on signaling by members of the NR superfamily.
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RA mobilizes to the nucleus through binding to small intracellular lipid-binding proteins.
“Basically, RA mobilizes to the nucleus through binding to small intracellular lipid-binding proteins.”
From Vitamin A and retinoid signaling: genomic and nongenomic effects (2013) · cites this paper as [5]
The Introduction (page not available) says cellular RA-binding proteins (CRABPs) mediate RA uptake in target cells, supporting a role for binding proteins in RA movement. It does not say they carry RA to the nucleus, so the claimed destination and transport mechanism are not established by this copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredRARs work as ligand-dependent regulators of transcription and transduce the RA signal in vivo as heterodimers with RXR.
“the so-called retinoic acid receptors (RAR), which work as ligand-dependent regulators of transcription and transduce the RA signal in vivo as heterodimers with retinoic X receptors (RXR) ( 5,6 ).”
From Vitamin A and retinoid signaling: genomic and nongenomic effects (2013) · cites this paper as [5]
RA binds and activates RARs.
“Today, it is well admitted that RA binds and activates RARs.”
From Vitamin A and retinoid signaling: genomic and nongenomic effects (2013) · cites this paper as [5]
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- Authors
- McKenna, N. J.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- McKenna, Neil J.
- ORCID
- McKenna, Neil J.
- Venue
- Nuclear Receptor Signaling
- Publisher
- SAGE Publications
- Published
- 2012-01
- Volume
- 10
- Issue
- 1
- Pages
- e003-e003
- ISSN
- 1550-7629 (ISSN-L)
- PMC
- PMC3309077
- OpenAlex
- W2092040763
- Cited by
- 33
- References
- 21
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 5 · 2013: 4
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Nuclear Receptor Signaling (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, other-oa)
- PubMed (publishedVersion)
- 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 › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- retinoic acid, retinoic acid receptor, retinoids, vitamin A metabolism, nuclear receptor superfamily, transcriptional regulation, coregulators, basal transcription machinery, retinoid signaling, breast cancer, hematologic malignancies, inflammatory diseases
- MeSH terms
- Animals, Congresses as Topic, Female, Humans, Tretinoin, Signal Transduction, Gene Expression, Receptors, Retinoic Acid, Gene Regulatory Networks
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