Anatomy of the estrogen response element

Gruber, Christian J.; Gruber, Doris; Gruber, Isabel M.L.; Wieser, Friedrich; Huber, Johannes

doi:10.1016/j.tem.2004.01.008

Cited by 266 publications

(184 citation statements)

References 60 publications

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“…These are all imperfect ERE sites because they do not contain canonical palindromic ERE sequences, yet they show half-ERE consensus sequences. Although it has been reported that half-ERE sites confer weak E 2 responsiveness, genes are known for which E 2 -induced transcription is mediated by two or more ERE half-sites [37]. The importance of these sites in mediating the E 2 effect on faah promoter activity has been investigated by mutant analysis, demonstrating that ERE2 and ERE3 are necessary for promoter stimulation by E 2 ; indeed, deletion of one of these sites or mutations in their sequence completely abolished the E 2 effect.…”

Section: Discussionmentioning

confidence: 99%

The faah gene is the first direct target of estrogen in the testis: role of histone demethylase LSD1

Grimaldi

Pucci

Siena

et al. 2012

Cell. Mol. Life Sci.

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Estrogen (E 2 ) regulates spermatogenesis, yet its direct target genes have not been identified in the testis. Here, we cloned the proximal 5 0 flanking region of the mouse fatty acid amide hydrolase (faah) gene upstream of the luciferase reporter gene, and demonstrated its promoter activity and E 2 inducibility in primary mouse Sertoli cells. Specific mutations in the E 2 response elements (ERE) of the faah gene showed that two proximal ERE sequences (ERE2/3) are essential for E 2 -induced transcription, and chromatin immunoprecipitation experiments showed that E 2 induced estrogen receptor b binding at ERE2/3 sites in the faah promoter in vivo. Moreover, the histone demethylase LSD1 was found to be associated with ERE2/3 sites and to play a role in mediating E 2 induction of FAAH expression. E 2 induced epigenetic modifications at the faah proximal promoter compatible with transcriptional activation by remarkably decreasing methylation of both DNA at CpG site and histone H3 at lysine 9. Finally, FAAH silencing abolished E 2 protection against apoptosis induced by the FAAH substrate anandamide. Taken together, our results identify FAAH as the first direct target of E 2 .

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Section: Discussionmentioning

confidence: 99%

The faah gene is the first direct target of estrogen in the testis: role of histone demethylase LSD1

Grimaldi

Pucci

Siena

et al. 2012

Cell. Mol. Life Sci.

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“…The nuclear-effects on a variety of tissues that involves gene stimulation as well as gene repression (Herbison, 1998, Couse and Korach, 1999, Nilsson et al, 2001, Stossi et al, 2006, Kininis et al, 2007. In general, this "classical" signaling pathway of estrogen involves steroid-dependent formation of nuclear estrogen receptor homo-or heterodimers and the subsequent binding of this complex with a unique DNA sequence known as an estrogen response element (ERE), in E2-responsive gene promoters (O'Malley and Tsai, 1992, Muramatsu and Inoue, 2000, Gruber et al, 2004. The inactive ER exists in a complex of several proteins that disassociate upon ligand binding, which transforms the receptor to an active state Korach, 1999, Gruber et al, 2004).…”

Section: Nuclear-initiated Signaling Of E2mentioning

confidence: 99%

“…Several genes in the brain that are clearly estrogen-responsive do not appear to contain ERE sequences (Malyala et al, 2004, Gruber et al, 2004. There is compelling evidence that ERα and ERβ can regulate transcription of some of these "estrogen-responsive" genes by interacting with other DNA-bound transcription factors, such as specificity protein-1 (SP-1) and activator protein 1 (AP-1), rather than binding directly to DNA (Paech et al, 1997, Jacobson et al, 2003, Gruber et al, 2004.…”

Section: Nuclear-initiated Signaling Of E2mentioning

confidence: 99%

“…There is compelling evidence that ERα and ERβ can regulate transcription of some of these "estrogen-responsive" genes by interacting with other DNA-bound transcription factors, such as specificity protein-1 (SP-1) and activator protein 1 (AP-1), rather than binding directly to DNA (Paech et al, 1997, Jacobson et al, 2003, Gruber et al, 2004. For example, the ligand-induced responses with ERβ, in contrast to ERα, at an AP-1 site illustrates the negative transcriptional regulation by estrogen and strong positive regulation by antiestrogens like ICI 164,384 (Paech et al, 1997).…”

Section: Nuclear-initiated Signaling Of E2mentioning

confidence: 99%

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Membrane-initiated estrogen signaling in hypothalamic neurons

Kelly

Rønnekleiv

2008

Molecular and Cellular Endocrinology

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SummaryIt is well known that many of the actions of 17β-estradiol (E2) in the central nervous system are mediated via intracellular receptor/transcription factors that interact with steroid response elements on target genes. However, there is compelling evidence for membrane steroid receptors for estrogen in hypothalamic and other brain neurons. But it is not well understood how estrogen signals via membrane receptors, and how these signals impact not only membrane excitability but also gene transcription in neurons. Indeed, it has been known for sometime that E2 can rapidly alter neuronal activity within seconds, indicating that some cellular effects can occur via membrane delimited events. In addition, E2 can affect second messenger systems including calcium mobilization and a plethora of kinases to alter cell signaling. Therefore, this review will consider our current knowledge of rapid membrane-initiated and intracellular signaling by E2 in the hypothalamus, the nature of receptors involved and how they contribute to homeostatic functions. KeywordsERα; ERβ; GPCR (G protein-coupled receptor); mER (membrane estrogen receptor that is a GPCR) Electrophysiological studies in the 1960's and 1970's suggested that gonadal steroids could directly modulate the electrical activity of hypothalamic neurons

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“…Estrogen mainly functions via estrogen receptor (ER␣ and ER␤), and ligand binding induces ER dimerization and translocation to nucleus where they recognize estrogen responsive element (ERE) in the promoters of target genes for transcription (Gruber et al, 2004). Besides this classical way, ligand-bound ER may recruit other transcription factors to modulate its functions in different tissues, and one of the well studied cofactor is activator protein-1 (AP-1) (Safe and Kim, 2008).…”

Section: Introductionmentioning

confidence: 99%