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Role of the aryl hydrocarbon receptor in cell cycle regulation
Abstract
Traditionally, the aryl hydrocarbon receptor (AHR) is considered to be a ligand-activated receptor and transcription factor responsible for the induction of drug-metabolizing enzymes. Its role in the combinatorial matrix of cell functions was neatly established long before the first report of an AHR cDNA sequence was published. Only recently, other functions of this protein have begun to be recognized. This review addresses novel findings relating to AHR functions that have resulted from experimental approaches markedly outside traditional receptor analyses. Here we examine the aspects of AHR biology relevant to its role in cell cycle regulation, from the activation of mitogen-activated protein kinases to the cross-talk between AHR and the RAS pathway and the functional significance of the interaction between AHR and the retinoblastoma protein. We have attempted to provide the reader with a balanced interpretation of the evidence, highlighting areas of consensus as well as areas still being contested.
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“Among the 15 fixed protein-coding changes identified here but absent from previous analyses1,20, some might have also contributed to complex modifications of pathways in cell division, like AHR65 or DNHD166 (Supplementary Information 1), as well as other genes with HHMCs, like CHEK167 or the gene encoding for the protein TOP2A68, which shows the largest number of interactions with other HHMC-carry”
From A catalog of single nucleotide changes distinguishing modern humans from archaic hominins (2019) · cites this paper as [65]
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Research works printed but not linked: 2
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Metadata
- Authors
- Puga, A., Xia, Y., & Elferink, C.
- Affiliations
- University of Cincinnati Medical Center (US)
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Puga, Alvaro
- Venue
- Chemico-Biological Interactions
- Publisher
- Elsevier BV
- Published
- 2002-09
- Volume
- 141
- Issue
- 1-2
- Pages
- 117-130
- ISSN
- 0009-2797 (ISSN-L)
- OpenAlex
- W2139905874
- Cited by
- 192
- References
- 83
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 6 · 2023: 4 · 2022: 6 · 2021: 6 · 2020: 8 · 2019: 6 · 2018: 3 · 2017: 5 · 2016: 5 · 2015: 8 · 2014: 5 · 2013: 10 · 2012: 11
- FWCI
- 8.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Chemico-Biological Interactions (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Environmental Health Sciences (R01ES007800, R01ES010807, ES10807, P30ES006096, R01 ES07800, R01ES006273, P30 ES-06096, R01 ES-06273)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Keywords
- aryl hydrocarbon receptor, cell cycle regulation, mitogen-activated protein kinase, Ras signaling, retinoblastoma protein, signal transduction, transcription factors, drug-metabolizing enzymes
- MeSH terms
- Animals, Cell Cycle, Gene Expression Regulation, Phosphorylation, Xenobiotics, Signal Transduction, Oncogene Proteins, Genes, Tumor Suppressor, Receptors, Aryl Hydrocarbon
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