Literature DB >> 29155216

Communication between genomic and non-genomic signaling events coordinate steroid hormone actions.

Sandi R Wilkenfeld1, Chenchu Lin2, Daniel E Frigo3.   

Abstract

Steroid hormones are lipophilic molecules produced in one cell that can travel great distances within the body to elicit biological effects in another cell. In the canonical pathway, steroid hormone binding to a nuclear receptor (NR), often in the cytoplasm, causes the receptor to undergo a conformational change and translocate to the nucleus, where it interacts with specific sequences of DNA to regulate transcription. In addition to the classical genomic mechanism of action, alternate mechanisms of steroid activity have emerged that involve rapid, non-genomic signaling. The distinction between these two major mechanisms of action lies in the subcellular location of the initiating steroid hormone action. Importantly, the mechanisms of action are not exclusive, in that each can affect the activity of the other. Here, we describe the different types of genomic and non-genomic steroid hormone signaling mechanisms and how they can influence one another to ultimately regulate biology. Further, we discuss the approaches being used to study the non-genomic signaling events and address important caveats to be considered when designing new experiments. Thus, this minireview can serve as an introduction to the diverse signaling mechanisms of steroid hormones and offers initial, experimental guidance to those entering the field.
Copyright © 2017 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Genomic; Non-genomic; Nuclear receptor; Rapid signaling; Steroid hormone; Subcellular localization

Mesh:

Substances:

Year:  2017        PMID: 29155216      PMCID: PMC5864526          DOI: 10.1016/j.steroids.2017.11.005

Source DB:  PubMed          Journal:  Steroids        ISSN: 0039-128X            Impact factor:   2.668


  72 in total

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Review 4.  Dissecting rapid estrogen signaling with conjugates.

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5.  Ca2+ channel subunit α 1D promotes proliferation and migration of endometrial cancer cells mediated by 17β-estradiol via the G protein-coupled estrogen receptor.

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6.  Rapid increase of spines by dihydrotestosterone and testosterone in hippocampal neurons: Dependence on synaptic androgen receptor and kinase networks.

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7.  Ligand-independent activation of the androgen receptor by interleukin-6 and the role of steroid receptor coactivator-1 in prostate cancer cells.

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Review 1.  Unconventional Estrogen Signaling in Health and Disease.

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Review 2.  Role of the glucocorticoid receptor in glomerular disease.

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Journal:  Am J Physiol Renal Physiol       Date:  2019-06-05

3.  Acute slice preparation for electrophysiology increases spine numbers equivalently in the male and female juvenile hippocampus: a DiI labeling study.

Authors:  J S Trivino-Paredes; P C Nahirney; C Pinar; P Grandes; B R Christie
Journal:  J Neurophysiol       Date:  2019-07-03       Impact factor: 2.714

Review 4.  The interaction of steroids with phospholipid bilayers and membranes.

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5.  Mechanosensitive Steroid Hormone Signaling and Cell Fate.

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Review 6.  Rapid effects of 17β-estradiol on aggressive behavior in songbirds: Environmental and genetic influences.

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7.  Mechanisms underlying suppression of noradrenaline-induced contraction by prolonged treatment with advanced glycation end-products in organ-cultured rat carotid artery.

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8.  Crosstalk between progesterone receptor membrane component 1 and estrogen receptor α promotes breast cancer cell proliferation.

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Review 9.  Androgen-induced epigenetic modulations in the ovary.

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Review 10.  Estrogen- and Progesterone (P4)-Mediated Epigenetic Modifications of Endometrial Stromal Cells (EnSCs) and/or Mesenchymal Stem/Stromal Cells (MSCs) in the Etiopathogenesis of Endometriosis.

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