Cited by 1,011Inflammatory mediators and NSAID effectsReceptor Mechanisms and SignalingEicosanoids and Hypertension Pharmacology

Prostanoid Receptors: Subtypes and Signaling

Breyer, Richard M, Bagdassarian, Carey K, Myers, Scott A, Breyer, Matthew D·2001·Annual Review of Pharmacology and Toxicology

Abstract

Cyclooxygenases metabolize arachidonate to five primary prostanoids: PGE 2, PGF 2α, PGI 2, TxA 2, and PGD 2. These autacrine lipid mediators interact with specific members of a family of distinct G-protein-coupled prostanoid receptors, designated EP, FP, IP, TP, and DP, respectively. Each of these receptors has been cloned, expressed, and characterized. This family of eight prostanoid receptor complementary DNAs encodes seven transmembrane proteins which are typical of G-protein-coupled receptors and these receptors are distinguished by their ligand-binding profiles and the signal transduction pathways activated on ligand binding. Ligand-binding selectivity of these receptors is determined by both the transmembrane sequences and amino acid residues in the putative extracellular-loop regions. The selectivity of interaction between the receptors and G proteins appears to be mediated at least in part by the C-terminal tail region. Each of the EP 1, EP 3, FP, and TP receptors has alternative splice variants described that alter the coding sequence in the C-terminal intracellular tail region. The C-terminal variants modulate signal transduction, phosphorylation, and desensitization of these receptors, as well as altering agonist-independent constitutive activity.

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Crossref · 10.1146/annurev.pharmtox.41.1.661

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  • PGE2 activates PKA signaling via raising intracellular cAMP, which can enhance binding of SF-1 to promoters of steroidogenic genes and induce phosphorylation of CREB.

    “PGE2 activates the protein kinase A (PKA) signaling pathway via raising the intracellular levels of cyclic adenosine 3′,5′-monophosphate (cAMP)12–14, which can enhance the binding of steroidogenic factor-1 (SF-1) to promoters of these steroidogenic genes15, and induce phosphorylation of the transcriptional activator cAMP-response element-binding protein (CREB)16.”

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Authors
Breyer, R. M., Bagdassarian, C. K., Myers, S. A., & Breyer, M. D.
Affiliations
United States Department of Veterans Affairs (US)
Venue
Annual Review of Pharmacology and Toxicology
Published
2001-04
Volume
41
Issue
1
Pages
661-690
ISSN
  • 0362-1642 (ISSN-L)
  • 1545-4304
OpenAlex
W2129746956
Cited by
1,011
References
152
Citations by year
2026: 7 · 2025: 17 · 2024: 11 · 2023: 22 · 2022: 17 · 2021: 27 · 2020: 37 · 2019: 22 · 2018: 24 · 2017: 32 · 2016: 38 · 2015: 43 · 2014: 50 · 2013: 40 · 2012: 51
FWCI
5.37
Type
journal article
Language
en
Open access
closed
Locations
  • The Annual Review of Pharmacology and Toxicology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of General Medical Sciences (GM 15431)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK37097, DK46205, R01DK037097, R01DK046205)
Topics
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
prostanoid receptors, G protein-coupled receptors, prostaglandins, cyclooxygenase, arachidonic acid metabolism, prostaglandin E2, prostaglandin F2alpha, prostacyclin, thromboxane A2, prostaglandin D2, receptor subtypes, ligand selectivity, splice variants, receptor desensitization, receptor phosphorylation, constitutive receptor activity, signal transduction
MeSH terms
Amino Acid Sequence, Animals, Humans, Molecular Sequence Data, Prostaglandins, Receptors, Prostaglandin, Signal Transduction

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