The DOI matches its Crossref record; 81 of the 83 references it cites were found in a registry or an index.
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]
Citations
Cites
CDK inhibitors: positive and negative regulators of G1-phase progression
Sherr, C. J., & Roberts, J. M. (1999) · Genes & Development · doi:10.1101/gad.13.12.1501 · Cited by 6,115
Barbacid, M. (1987) · Annual Review of Biochemistry · doi:10.1146/annurev.bi.56.070187.004023 · Cited by 3,885
Cheng, M., Olivier, P., Diehl, J. A., Fero, M., Roussel, M. F., Roberts, J. M., & Sherr, C. J. (1999) · The EMBO Journal · doi:10.1093/emboj/18.6.1571 · Cited by 1,142
Molecular Interaction Map of the Mammalian Cell Cycle Control and DNA Repair Systems
Kohn, K. W. (1999) · Molecular Biology of the Cell · doi:10.1091/mbc.10.8.2703 · Cited by 561
Induction of c‐fos expression through JNK‐mediated TCF/Elk‐1 phosphorylation.
Cavigelli, M., Dolfi, F., Claret, F. X., & Karin, M. (1995) · The EMBO Journal · doi:10.1002/j.1460-2075.1995.tb00284.x · Cited by 530
Differential Phosphorylation of the Retinoblastoma Protein by G1/S Cyclin-dependent Kinases
Zarkowska, T., & Mittnacht, S. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.19.12738 · Cited by 494
Mechanism of active transcriptional repression by the retinoblastoma protein
Weintraub, S. J., Chow, K. N. B., Luo, R. X., Zhang, S. H., He, S., & Dean, D. C. (1995) · Nature · doi:10.1038/375812a0 · Cited by 487
Ah Receptor and NF-κB Interactions, a Potential Mechanism for Dioxin Toxicity
Tian, Y., Ke, S., Denison, M. S., Rabson, A. B., & Gallo, M. A. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.1.510 · Cited by 406
Kolluri, S. K., Weiss, C., Koff, A., & Göttlicher, M. (1999) · Genes & Development · doi:10.1101/gad.13.13.1742 · Cited by 364
Checking out the G2/M transition
Smits, V. A. J., & Medema, R. H. (2001) · Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression · doi:10.1016/s0167-4781(01)00204-4 · Cited by 359
Research works printed but not linked: 2
- A. Puga, J. Bohm, A. Hoffer, G.D. Leikauf, H.G. Shertzer, S. Zhou, Dioxin alters calcium homeostasis and the regulation of arachidonate metabolism in mouse hepatoma cells, Proceedings of the 15th International Symposium on Chlorinated Dioxins, vol. 25, 1995, pp. 381–386.
- Reiners, 1997, Downregulation of aryl hydrocarbon receptor function and cytochrome P450 1A1 induction by expression of Ha-ras oncogenes, Mol. Carcinog., 19, 91, 10.1002/(SICI)1098-2744(199707)19:2<91::AID-MC4>3.0.CO;2-O · DOI
Cited by
Sorted by citations
The aryl hydrocarbon receptor: multitasking in the immune system
Stockinger, B., Meglio, P. D., Gialitakis, M., & Duarte, J. H. (2014) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032713-120245 · Cited by 909
Aryl hydrocarbon receptor ligands in cancer: friend and foe
Murray, I. A., Patterson, A. D., & Perdew, G. H. (2014) · Nature reviews. Cancer · doi:10.1038/nrc3846 · Cited by 916
The Aryl Hydrocarbon Receptor Complex and the Control of Gene Expression
Beischlag, T. V., Morales, J. L., Hollingshead, B. D., & Perdew, G. H. (2008) · Critical Reviews™ in Eukaryotic Gene Expression · doi:10.1615/critreveukargeneexpr.v18.i3.20 · Cited by 727
The aryl hydrocarbon receptor cross-talks with multiple signal transduction pathways
Puga, A., Ma, C., & Marlowe, J. L. (2008) · Biochemical Pharmacology · doi:10.1016/j.bcp.2008.08.031 · Cited by 409
Self-citationAh receptor: Dioxin-mediated toxic responses as hints to deregulated physiologic functions
Bock, K. W., & Köhle, C. (2006) · Biochemical Pharmacology · doi:10.1016/j.bcp.2006.01.017 · Cited by 340
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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