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Introduction The most potent and active estrogen in humans is 17β-estradiol (E 2 ), and the biological effects of E 2 are mediated through its binding to estrogen receptor (ER)α and ERβ. E 2 -bound ER acts via genomic and non-genomic mechanisms
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. ERα and ERβ have both overlapping and unique functions ( Matthews & Gustafsson 2003 ), and ERβ is thought to act as an inhibitor of ERα activity ( Hall & McDonnell 1999 ). Knowledge of the tissue-specific expression and the subsequent role of ERα and
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fingerprint of 17β-estradiol was observed when an inducible genetic construct was used to express, in addition to ERα, also the ERβ subtype. Materials and methods Chemicals Daidzein and resveratrol were purchased from Sigma–Aldrich; 17β-estradiol, coumestrol
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said to convert ERα-positive tumors from good to poor prognosis ( Kenny et al. 1999 ). The cyclin D1 gene is shown to physically associate with the ER and induce ER signaling in a cdk-independent manner ( Zwijsen et al. 1997 ). Immuno
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Introduction Nuclear estrogen receptors alpha (ERα) represent almost the first molecular targets used for breast cancer treatment, and two-thirds of these patients are treated with an endocrine therapy. Nuclear progesterone receptors (PRs) on
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immunoblotting and immunohistochemistry, and was non-cross-reactive with EGR1, EGR2, or Wilms’ tumor proteins (data from Santa Cruz Bio-technology). Monoclonal antibodies for ERα (ER1D5), progesterone receptor (PR; MAB429), and Ki-67 (MIB1) were purchased from
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homeostasis. 17β-Estradiol (E2) binding to the cytosolic ER population (both ERα and ERβ) induces conformational changes that facilitate ER homo/heterodimerization, nuclear translocation, and binding to specific DNA recognition sequences (i.e. estrogen
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Introduction The estrogen receptor α (ERα) plays a crucial role in the clinical care of breast cancer patients, and measurement of the level of ERα expression has allowed an accurate prediction of the response to endocrine therapy
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influence how we proceed in the future. Session 1 focused around oestrogen receptor-α (ERα) as an old target that has recently spawned the exciting third generation of aromatase inhibitors and where new knowledge of the molecular actions of the ER is
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Two oestrogen receptors (ERs) coded on different genes have been identified – ERα and ERβ – although numerous mRNA splice variants exist for these receptors in both diseased and normal tissue ( Moore et al. 1998 , Flouriot et al. 2000 , Deroo
