Steroid hormone receptors: Many Actors in search of a plot

Beato, Miguel; Herrlich, Peter; Schütz, Günther

doi:10.1016/0092-8674(95)90201-5

Cited by 1,695 publications

(1,089 citation statements)

References 51 publications

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“…Their known e ects are mediated by a cytoplasmic androgen receptor (AR) that is translocated into the nucleus upon hormone binding to positively or negatively modulate the expression of speci®c genes (Beato et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

“…The ability to regulate gene expression positively and negatively is not speci®c to the AR but is shared by other steroid receptors (Beato et al, 1995). In addition, a number of steroid hormones are reported to rapidly and reversibly activate important intermediates in signal transduction pathways known to trigger cell proliferation (Migliaccio et al, , 1998Endoh et al, 1997;Marcinkowska et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Rapid signalling by androgen receptor in prostate cancer cells

Peterziel¹,

Mink²,

Schonert³

et al. 1999

Oncogene

236

157

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Androgens are important growth regulators in prostate cancer. Their known mode of action in target cells requires binding to a cytoplasmic androgen receptor followed by a nuclear translocation event and modulation of the expression of speci®c genes. Here, we report another mode of action of this receptor. Treatment of androgen responsive prostate cancer cells with dihydrotestosterone leads to a rapid and reversible activation of mitogen-activated protein kinases MAPKs (also called extracellular signal-regulated kinases or Erks). Transient transfection assays demonstrated that the androgen receptor-mediated activation of MAP kinase results in enhanced activity of the transcription factor Elk-1. This action of the androgen receptor di ers from its known transcriptional activity since it is rapid and insensitive to androgen antagonists such as hydroxy¯utamide or casodex. Biochemical studies as well as analyses with dominant negative mutants showed the involvement of kinases such as MAPK/Erk kinase, phosphatidyl-inositol 3-kinase and protein kinase C in the androgen receptormediated activation of MAP kinase. These results demonstrate a novel regulatory action of the androgen receptor and prove that in addition to its known transcriptional e ects, it also uses non-conventional means to modulate several cellular signalling processes.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Rapid signalling by androgen receptor in prostate cancer cells

Peterziel¹,

Mink²,

Schonert³

et al. 1999

Oncogene

236

157

View full text Add to dashboard Cite

show abstract

“…The classical genomic pathway involves direct DNA binding of E2‐ER to oestrogen response elements (EREs)36 in the promoter regions of target genes 37. The alternate, nonclassical genomic pathway involves the indirect modulation of transcription by the interaction of the ER with other transcription complexes, such as AP‐1, SP1 and NF‐κB 37.…”

Section: Discussionmentioning

confidence: 99%

Regulation of TRPV5 transcription and expression by E2/ERα signalling contributes to inhibition of osteoclastogenesis

Song

Lin

et al. 2018

J Cellular Molecular Medi

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The increasing of osteoclasts formation and activity because of oestrogen (E2) deficiency is very important in the aetiology of postmenopausal osteoporosis. Our previous studies showed that E2 inhibited osteoclastic bone resorption by increasing the expression of Transient Receptor Potential Vanilloid 5 (TRPV5) channel. However, the exact mechanism by which E2 increases TRPV5 expression is not fully elucidated. In this study, Western blot, quantitative real‐time PCR, tartrate‐resistant acid phosphatase staining, F‐actin ring staining, chromatin immunoprecipitation and luciferase assay were applied to explore the mechanisms that E2‐induced TRPV5 expression contributes to the inhibition of osteoclastogenesis. The results showed that silencing or overexpressing of TRPV5 significantly affected osteoclasts differentiation and activity. Silencing of TRPV5 obviously alleviated E2‐inhibited osteoclastogenesis, resulting in increasing of bone resorption. E2 stimulated mature osteoclasts apoptosis by increasing TRPV5 expression. Further studies showed that E2 increased TRPV5 expression through the interaction of the oestrogen receptor α (ERα) with NF‐κB, which could directly bind to the fragment of −286 nt ~ −277 nt in the promoter region of trpv5. Taken together, we conclude that TRPV5 plays a dominant effect in E2‐mediated osteoclasts formation, bone resorption activity and osteoclasts apoptosis. Furthermore, NF‐κB plays an important role in the transcriptional activation of E2‐ERα stimulated TRPV5 expression.

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“…In this manner, the action of MAPKs and protein phosphatases reciprocally and rapidly alter the behavior of cells as they respond to changes in their environment. MAPK activity is regulated through three-tiered cascades composed of a MAPK, MKK or MAPKK and MEKK or MAPKKK (Beato et al 1995). A MAPKKK that is activated by extracellular stimuli phosphorylates a MAPKK on its serine and threonine residues.…”

Section: Erk5 and Jnk Cascades As A System Of Interacting Proteinsmentioning

confidence: 99%

Lose and gain: impacts of ERK5 and JNK cascades on each other

Pandurangan

Gakkhar

2010

Syst Synth Biol

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Kinase cascades in ERK5 (Extracellular signalregulated kinases) and JNK (c-Jun N-terminal kinases) signaling pathways mediate the sensing and processing of stimuli. Cross-talks between signaling cascades is a likely phenomenon that can cause apparently different biological responses from a single pathway, on its activation. Feedback loops have the potential to greatly alter the properties of a pathway and its response to stimuli. Based on enzyme kinetic reactions, mathematical models have been developed to predict and analyze the impacts of cross-talks and feedback loops in ERK5 and JNK cascades. It has been observed that, there is no significant impact on neither ERK5 activation nor JNKs' activation due to cross-talks between them. But it is due to cross-talks and feedback loops in ERK5 and JNK cascade, ERK5 gets activated in a transient manner in the absence of input signals. Planning to obtain the parameter values from the experimentalist and the result should be validated by experimental verification.

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Steroid hormone receptors: Many Actors in search of a plot

Cited by 1,695 publications

References 51 publications

Rapid signalling by androgen receptor in prostate cancer cells

Rapid signalling by androgen receptor in prostate cancer cells

Regulation of TRPV5 transcription and expression by E2/ERα signalling contributes to inhibition of osteoclastogenesis

Lose and gain: impacts of ERK5 and JNK cascades on each other

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