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Example sentences for: cres
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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.
Calmodulin PDEs (CaM-PDEs) are sensitive to calmodulin and calcium up regulation [ 54 ] . cAMP can then affect cell signaling via interactions with the regulatory subunits of cAMP activated kinases, including protein kinase A, leading to their subsequent activation, and via binding of cAMP response element binding proteins (CREBs) to cAMP response elements (CREs) or cAMP response units (CRU) consisting of CREs.
Both ERs enhance transcription from genes with classical estrogen response elements (EREs), but ERα requires less ligand to obtain maximal activation than ERβ [ 25 26 ] . Likewise, both ERs suppress the activity of the TNFα promoter in response to estrogens, but ERβ is a more potent repressor than ERα [ 27 ] . However, some of the most striking isoform-specific differences in gene regulation are observed at promoters, such as that of cyclin D1, which contain AP-1 sites or related cyclic AMP response elements (CREs).
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