title: Nuclear estrogen receptors co-activation mechanisms.
abstract: 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.
authors: Dept. of Synthesis and Chemical Technology of Pharmaceutical Substances, Faculty of Pharmacy, Medical University of Lublin, Poland.
authors: M
authors: M
authors: Skrzypczak
authors: L
authors: L
authors: Kapka-Skrzypczak
authors: M
authors: M
authors: Cyranka
authors: O
authors: O
authors: Treeck
authors: A
authors: A
authors: Wrobel
authors: D
authors: D
authors: Matosiuk
mesh_terms: D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D047628:Estrogen Receptor alpha / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D047629:Estrogen Receptor beta / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D004967:Estrogens / Q000737:chemistry / Q000378:metabolism; D051548:Histone Acetyltransferases / Q000378:metabolism; D006801:Humans; D010766:Phosphorylation; D000091402:Prohibitins; D011485:Protein Binding; D011493:Protein Kinase C / Q000378:metabolism; D018336:Receptors, Aryl Hydrocarbon / Q000737:chemistry / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000737:chemistry / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D015398:Signal Transduction; D000097983:ERRalpha Estrogen-Related Receptor
chemical_list: D017868:Cyclic AMP-Dependent Protein Kinases; D004247:DNA; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D004967:Estrogens; D051548:Histone Acetyltransferases; D000091402:Prohibitins; D011493:Protein Kinase C; D018336:Receptors, Aryl Hydrocarbon; D018160:Receptors, Cytoplasmic and Nuclear; D011960:Receptors, Estrogen; D000097983:ERRalpha Estrogen-Related Receptor; C000717331:PHB2 protein, human