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Example sentences for: serms
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2shows that the ERβ-LBD bound N-CoR in the presence of agonists and phytoestrogens, but not SERMs.
Provocative mechanistic connections have been made between the steroid hormone superfamily, including the SERMS and retinoids, and the TGF-β family of multifunctional growth factors [ 8].
Thus, ERβ binds the N-CoR C-terminal NR interacting region in the presence of agonists, but not SERMs, and does so in vitro and in mammalian cells.
ERα enhances AP-1 activity in response to estrogens, [ 28 29 ] but ERβ inhibits AP-1 activity in response to estrogens [ 29 30 31 ] . ERβ also completely suppresses ERα activity at the cyclin D1 promoter and even suppresses the activity of an ERα mutant that is selectively superactive at AP-1 sites and CREs [ 29 ] . Finally, ERβ shows a unique capacity to enhance AP-1 activity in response to selective estrogen receptor modulators (SERMs) such as raloxifene, tamoxifen and ICI 182,780/Faslodex (ICI) [ 30 31 32 ] . Together, these observations suggest that there are fundamental differences in the way that the ERs bind unspecified cofactors that modulate gene expression, and that some of these cofactors must play a role in differential ER activity at AP-1 sites.
While the ER isoforms have contrasting effects on AP-1 activity in the presence of estrogens, ERα truncations that lack the NTD and ERβ both enhance AP-1 activity in the presence of SERMs [ 30 31 ] . Mutational analysis of ERα action at AP-1 sites suggests these effects may be related to N-CoR binding [ 39 ] , and we have proposed that SERM action at AP-1 sites may therefore involve contacts with corepressors [ 31 51 ] . The fact that ERα and ERβ show completely different ligand preferences of interaction with N-CoR suggests that the target for SERM activation at AP-1 sites may not be N-CoR in both cases.
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