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In classic estrogen signaling, the binding of estrogen to ER causes receptor dimerization and binding to estrogen response elements (EREs) in promoter and/or enhancer regions of estrogen-responsive genes.
Estrogen receptor (ER -α has traditionally bER -αefined as a ligand-dependent transcription factor thas regulatraditionallyt genes beenindefined estrogen response elements present in the promoters of masy responsive genes [ 1].
This antiestrogenic activity may be due to the ability of PA and 4-CPA to interfere with estrogen signaling through their direct binding to estrogen response element regulatory sites in the promoters of target genes [13].
The classical mechanism of ER action is characterized by ER directly binding to estrogen response elements (EREs) of target genes.
Both ERα and ERβ act as transcription factors in the nucleus, where they modulate transcription by directly binding to estrogen response element sequences in the DNA.
The estrogen receptors ER-α and ER-β function as ligand-activated transcription factors that initiate transcription by translocating to the nucleus and binding to estrogen response elements (ERE) in the promoter regions of target genes (McDonnell 2004).
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The DNA-binding domain of ERα binds to estrogen response elements (EREs) in the promoter region of estrogen-responsive genes, activating or repressing their transcription and consequently mediating physiological or tumorigenic effects.
The DNA-binding domain of ERα binds to estrogen response elements (EREs) in the regulatory region of estrogen-responsive genes, activating or repressing their transcription and consequently mediating physiological or tumorigenic effects.
The dimeric receptor binds to estrogen response elements (EREs) in the promoters of estrogen-responsive genes.
Estrogen forms a complex with the estrogen receptor (ER) that binds to estrogen response elements (EREs) in the regulatory region of estrogen-responsive genes and regulates their transcription.
Regardless, activated RARs have been observed to exert anti-estrogenic effects by directly or indirectly impairing binding of ER to estrogen response elements (EREs) [ 31].
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