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Rapid actions of steroid receptors in cellular signaling pathways.
Sci STKE. 2002 Jun 25; 2002(138):re9.SS

Abstract

Steroid hormones regulate cellular processes by binding to intracellular receptors that, in turn, interact with discrete nucleotide sequences to alter gene expression. Because most steroid receptors in target cells are located in the cytoplasm, they need to get into the nucleus to alter gene expression. This process typically takes at least 30 to 60 minutes. In contrast, other regulatory actions of steroid hormones are manifested within seconds to a few minutes. These time periods are far too rapid to be due to changes at the genomic level and are therefore termed nongenomic or rapid actions, to distinguish them from the classical steroid hormone action of regulation of gene expression. The rapid effects of steroid hormones are manifold, ranging from activation of mitogen-activated protein kinases (MAPKs), adenylyl cyclase (AC), protein kinase C (PKC), and heterotrimeric guanosine triphosphate-binding proteins (G proteins). In some cases, these rapid actions of steroids are mediated through the classical steroid receptor that can also function as a ligand-activated transcription factor, whereas in other instances the evidence suggests that these rapid actions do not involve the classical steroid receptors. One candidate target for the nonclassical receptor-mediated effects are G protein-coupled receptors (GPCRs), which activate several signal transduction pathways. One characteristic of responses that are not mediated by the classical steroid receptors is insensitivity to steroid antagonists, which has contributed to the notion that a new class of steroid receptors may be responsible for part of the rapid action of steroids. Evidence suggests that the classical steroid receptors can be localized at the plasma membrane, where they may trigger a chain of reactions previously attributed only to growth factors. Identification of interaction domains on the classical steroid receptors involved in the rapid effects, and separation of this function from the genomic action of these receptors, should pave the way to a better understanding of the rapid action of steroid hormones.

Authors+Show Affiliations

Forschungszentrum Karlsruhe, Institute of Toxicology and Genetics, Post Office Box 3640, D-76021 Karlsruhe, Germany. andrew.cato@igen.fzk.deNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

12084906

Citation

Cato, Andrew C B., et al. "Rapid Actions of Steroid Receptors in Cellular Signaling Pathways." Science's STKE : Signal Transduction Knowledge Environment, vol. 2002, no. 138, 2002, pp. re9.
Cato AC, Nestl A, Mink S. Rapid actions of steroid receptors in cellular signaling pathways. Sci STKE. 2002;2002(138):re9.
Cato, A. C., Nestl, A., & Mink, S. (2002). Rapid actions of steroid receptors in cellular signaling pathways. Science's STKE : Signal Transduction Knowledge Environment, 2002(138), re9.
Cato AC, Nestl A, Mink S. Rapid Actions of Steroid Receptors in Cellular Signaling Pathways. Sci STKE. 2002 Jun 25;2002(138):re9. PubMed PMID: 12084906.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rapid actions of steroid receptors in cellular signaling pathways. AU - Cato,Andrew C B, AU - Nestl,Andrea, AU - Mink,Sigrun, Y1 - 2002/06/25/ PY - 2002/6/27/pubmed PY - 2002/7/13/medline PY - 2002/6/27/entrez SP - re9 EP - re9 JF - Science's STKE : signal transduction knowledge environment JO - Sci STKE VL - 2002 IS - 138 N2 - Steroid hormones regulate cellular processes by binding to intracellular receptors that, in turn, interact with discrete nucleotide sequences to alter gene expression. Because most steroid receptors in target cells are located in the cytoplasm, they need to get into the nucleus to alter gene expression. This process typically takes at least 30 to 60 minutes. In contrast, other regulatory actions of steroid hormones are manifested within seconds to a few minutes. These time periods are far too rapid to be due to changes at the genomic level and are therefore termed nongenomic or rapid actions, to distinguish them from the classical steroid hormone action of regulation of gene expression. The rapid effects of steroid hormones are manifold, ranging from activation of mitogen-activated protein kinases (MAPKs), adenylyl cyclase (AC), protein kinase C (PKC), and heterotrimeric guanosine triphosphate-binding proteins (G proteins). In some cases, these rapid actions of steroids are mediated through the classical steroid receptor that can also function as a ligand-activated transcription factor, whereas in other instances the evidence suggests that these rapid actions do not involve the classical steroid receptors. One candidate target for the nonclassical receptor-mediated effects are G protein-coupled receptors (GPCRs), which activate several signal transduction pathways. One characteristic of responses that are not mediated by the classical steroid receptors is insensitivity to steroid antagonists, which has contributed to the notion that a new class of steroid receptors may be responsible for part of the rapid action of steroids. Evidence suggests that the classical steroid receptors can be localized at the plasma membrane, where they may trigger a chain of reactions previously attributed only to growth factors. Identification of interaction domains on the classical steroid receptors involved in the rapid effects, and separation of this function from the genomic action of these receptors, should pave the way to a better understanding of the rapid action of steroid hormones. SN - 1525-8882 UR - https://www.unboundmedicine.com/medline/citation/12084906/Rapid_actions_of_steroid_receptors_in_cellular_signaling_pathways_ DB - PRIME DP - Unbound Medicine ER -