Dissecting the molecular mechanism of nuclear receptor action: transcription coactivators and corepressors

Lee, Jae Woon; Cheong, Jae Hun; Lee, Young Chul; Na, Soon Young; Lee, Soo Kyung

doi:10.1038/emm.2000.10

Cited by 6 publications

(4 citation statements)

References 68 publications

(64 reference statements)

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“…In addition to ERs, ER-coactivators are integral components of estrogen-dependent gene activation (Lee et al 2000; Lee et al 2001). During activation of estradiol-responsive genes, ERs interact with various ER-coregulators that bridge ERs to chromatin modifying proteins and basal transcription machinery and that ultimately lead to gene activation (Mangelsdorf et al 1995; Horwitz et al 1996; Nilsson and Gustafsson 2002; Lonard and O’Malley 2005; Chen et al 2006).…”

Section: Resultsmentioning

confidence: 99%

“…MLLs are well recognized histone 3 lysine (H3K4) specific histone methyltransferases that aid in gene activation (Hess 2004; Ansari et al 2009b; Ansari et al 2012b). MLLs possess multiple LXXLL domains (also called nuclear receptor box or NR box) through which they may interact with NRs and thus, participate in NR-mediated gene activation (Lee et al 2000; Lee et al 2001; Dreijerink et al 2006; Ansari and Mandal 2010). …”

Section: Resultsmentioning

confidence: 99%

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Bisphenol-A and diethylstilbestrol exposure induces the expression of breast cancer associated long noncoding RNA HOTAIR in vitro and in vivo

Bhan

Hussain

Ansari

et al. 2014

The Journal of Steroid Biochemistry and Molecular Biology

154

121

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Antisense transcript, long non-coding RNA HOTAIR is a key player in gene silencing and breast cancer and is transcriptionally regulated by estradiol. Here, we have investigated if HOTAIR expression is misregulated by bisphenol-A (BPA) and diethylstilbestrol (DES). Our findings demonstrate BPA and DES induce HOTAIR expression in cultured human breast cancer cells (MCF7) as well as in vivo in the mammary glands of rat. Luciferase assay showed that HOTAIR promoter estrogen-response-elements (EREs) are induced by BPA and DES. Estrogen-receptors (ERs) and ER-coregulators such as MLL-histone methylases (MLL1 and MLL3) bind to the HOTAIR promoter EREs in the presence of BPA and DES, modify chromatin (histone methylation and acetylation) and lead to gene activation. Knockdown of ERs down-regulated the BPA and DES induced expression of HOTAIR. In summary, our results demonstrate that BPA and DES exposure alters the epigenetic programming of the HOTAIR promoters leading to its endocrine disruption in vitro and in vivo.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Bisphenol-A and diethylstilbestrol exposure induces the expression of breast cancer associated long noncoding RNA HOTAIR in vitro and in vivo

Bhan

Hussain

Ansari

et al. 2014

The Journal of Steroid Biochemistry and Molecular Biology

154

121

View full text Add to dashboard Cite

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“…Histones are acetylated by histone acetyltransferase (HAT). Coactivators of the VDR such as p160 or p300/CBP, all have HAT activity to promote transcription in the presence of 1,25(OH) 2 D [118][119][120][121]. Conversely, histone deacetylation by histone deacetylase enzymes (HDACs) reverses this process to decrease gene transcription.…”

Section: Dvd Deficiency Genomic and Epigenetic Mechanismsmentioning

confidence: 99%

Vitamin D and schizophrenia: 20 years on

et al. 2021

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Many epidemiological studies have highlighted the link between vitamin D deficiency and schizophrenia. In particular, two prominent studies report an association between neonatal vitamin D deficiency and an increased risk of schizophrenia. In parallel, much has been learnt about the role of vitamin D in the developing central nervous system over the last two decades. Studies in rodent models of developmental vitamin D (DVD)-deficiency describe how brain development is altered leading to a range of neurobiological and behavioral phenotypes of interest to schizophrenia. While glutamate and gamma aminobutyric acid (GABA) systems have been little investigated in these models, alterations in developing dopamine systems are frequently reported. There have been far more studies reporting patients with schizophrenia have an increased risk of vitamin D deficiency compared to well controls. Here we have conducted a systematic review and meta-analysis that basically confirms this association and extends this to first-episode psychosis. However, patients with schizophrenia also have poorer general health, poorer diets, are frequently less active and also have an increased risk of other medical conditions, all factors which reduce circulating vitamin D levels. Therefore, we would urge caution in any causal interpretation of this association. We also summarize the inconsistent results from existing vitamin D supplementation trials in patients with schizophrenia. In respect to animal models of adult vitamin D deficiency, such exposures produce subtle neurochemical alterations and effects on cognition but do not appear to produce behavioral phenotypes of relevance to schizophrenia. We conclude, the hypothesis that vitamin D deficiency during early life may increase the risk of schizophrenia remains plausible and warrants ongoing research.

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“…Most of these cofactors are expressed in a wide variety of cell types and can interact with more than one type of nuclear receptor. The recent findings that members of the several different families of coactivators possess intrinsic histone acetyltransferase activity suggests that activated SHRs, and nuclear receptors in general, may also recruit these cofactors to remodel chromatin structure for better accessibility of the transcriptional machinery to DNA [5,6]. …”

Section: Introductionmentioning

confidence: 99%

Stat3 enhances transactivation of steroid hormone receptors

et al. 2003

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Background: Steroid hormone receptors (SHRs) are members of the superfamily of ligandactivated transcription factors that regulate many biological processes. Co-regulators act as bridging molecules between the SHR and general transcription factors to enhance transactivation of target genes. Previous studies demonstrated that Stat3 is constitutively activated in prostate cancer and can enhance prostate specific antigen (PSA) expression and promote androgen independent growth. In this study, we investigate whether Stat3 can enhance steroid hormone receptors activation.

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Dissecting the molecular mechanism of nuclear receptor action: transcription coactivators and corepressors

Cited by 6 publications

References 68 publications

Bisphenol-A and diethylstilbestrol exposure induces the expression of breast cancer associated long noncoding RNA HOTAIR in vitro and in vivo

Bisphenol-A and diethylstilbestrol exposure induces the expression of breast cancer associated long noncoding RNA HOTAIR in vitro and in vivo

Vitamin D and schizophrenia: 20 years on

Stat3 enhances transactivation of steroid hormone receptors

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