Estrogens play very important role in opening the transcription event, which is a final step of activation of the
first order mediators as receptors or channels in the cell wall by information coming from the outside of the cell. For the
long time the exact step by step mechanism of cellular transfer of information to the cell nuclei was not known. Currently
many new informations are available. Very important seems the step of phosphorylation and therefore desensitization of
the target proteins. All peptide kinases, especially serine and threonine, like protein kinases A and C, RAS and MAP
kinases, cycline kinases are potential or confirmed biological targets. Except them elements of the transcription complexes
like p160.SRC-1, histon acetyltransferase and histon deacetylase, CBP/p300, TRAP/DRIP, NSD1, PPARγ/PGC-1,
NCOR1, SMRT, REA were also found useful. Finally estrogens are able to activate other receptors, namely aryl hydrocarbon
receptors (AhR) and estrogen receptor related proteins (ERR). It is well known that many types of cancer are related
to the direct or indirect excessive activation of nuclear estrogen receptors, therefore their inhibition could be crucial
in many estrogen-related cancers. Understanding the interactions in such complexes would help in developing new and
better multi-target cures and finding new ligands with better pharmacological and pharmacokinetic properties.
Keywords: Estrogene receptors, estrogen co-activators, estrogen co-repressors, MAPK, histone acetyltransferase, histone
deacetylase, aromatic hydrocarbon receptor, estrogen receptor related proteins, protein kinases, cyclase kinases, kinase inhibitors.
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