The Expanding Complexity of Estrogen Receptor Signaling in the Cardiovascular System

The Expanding Complexity of Estrogen Receptor Signaling in the Cardiovascular System

Sara Menazza, Elizabeth Murphy

Genomic estrogen receptor (ER) signaling. A, Direct binding to DNA. Estrogen binding to ERs promotes receptor translocation to the nuclei. ERs bind to the consensus estrogen response element (ERE) in the DNA, mediating its genomic effects. Coactivators and corepressors are recruited to activate or inhibit gene. B, Indirectly binding DNA through other transcription factors. ERs can tether transcription factors (TF) such as API and Sp1 regulating gene expressions. C and D, Ligand-independent binding. ERs can be phosphorylated by kinases signaling (such as p38, extracellular-signal-regulated kinase [ERK], and activation of protein kinase B [Akt]) activated by plasma membrane ERs signaling. Specific serine site phosphorylation of ERs can trigger its binding to DNA, thus activating the transcription via ligand-independent binding or via ERE-binding. MAPK indicates mitogen-activated protein kinase; and PI3K, phosphatidylinositol-3-OH kinase. [Powerpoint File]

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