Ah receptor signals cross-talk with multiple developmental pathways
Biochemical Pharmacology, ISSN: 0006-2952, Vol: 69, Issue: 2, Page: 199-207
2005
- 149Citations
- 62Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations149
- Citation Indexes148
- 148
- CrossRef132
- Patent Family Citations1
- Patent Families1
- Captures62
- Readers62
- 62
- Mentions1
- References1
- Wikipedia1
Article Description
For many years, the Ah receptor (AHR) has been a favorite of toxicologists and molecular biologists studying the connections between genes and the changes in the control of gene expression resulting from environmental exposures. Much of the attention given to the Ah receptor has focused on the nature of its ligands, many of which are known or suspected carcinogens, and on the role that its best studied regulatory product, the CYP1A1 enzyme, plays in toxic responses and carcinogen activation. This understandable bias has resulted in a disproportionate amount of Ah receptor research being directed at toxicological or adaptive end points. In recent times, it has become evident that Ah receptor functions are also involved in molecular cascades that lead to inhibition of proliferation, promotion of differentiation, or apoptosis, with an important bearing in development. Developmental and toxicological AHR functions may not always be related. The ancestral AHR protein in invertebrates directs the developmental fate of a few specific neurons and does not bind xenobiotic ligands. The mammalian AHR maintains normal liver function in the absence of exogenous ligands and, when activated by dioxin, cross-talks with morphogenetic and developmental signals. Toxic end points, such as the induction of cleft palate by dioxin in mice embryos, might be at the crossroads of these signals and provide important clues as to the developmental role of the AHR.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006295204004605; http://dx.doi.org/10.1016/j.bcp.2004.06.043; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=13844298239&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15627472; https://linkinghub.elsevier.com/retrieve/pii/S0006295204004605; https://dx.doi.org/10.1016/j.bcp.2004.06.043
Elsevier BV
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