Dynamic transcriptional events mediated by estrogen receptor alpha

Ayaz G., Yasar P., OLGUN Ç. E., Karakaya B., Kars G., Razizadeh N., ...Daha Fazla

FRONTIERS IN BIOSCIENCE-LANDMARK, cilt.24, ss.245-276, 2019 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 24
  • Basım Tarihi: 2019
  • Doi Numarası: 10.2741/4716
  • Dergi Adı: FRONTIERS IN BIOSCIENCE-LANDMARK
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.245-276
  • Anahtar Kelimeler: Estrogen, Estrogen Receptor, Molecular Mechanism, Signaling, Structure, Review, DNA-BINDING DOMAIN, NUCLEAR HORMONE-RECEPTORS, EPIDERMAL-GROWTH-FACTOR, GENOME-WIDE ANALYSIS, BREAST-CANCER CELLS, ER-ALPHA, RESPONSE ELEMENT, ACTIVATION FUNCTION, DEPENDENT TRANSCRIPTION, CRYSTAL-STRUCTURE
  • Orta Doğu Teknik Üniversitesi Adresli: Evet

Özet

17beta-estradiol (E2), the main circulating estrogen hormone, is involved in a wide variety of physiological functions ranging from the development to the maintenance of many tissues and organs. The effects of E2 on cells are primarily conveyed by the transcription factors, estrogen receptor (ER) alpha and beta. The regulation of responsive genes by the well-defined ER alpha in response to E2 relies on complex and highly organized processes that dynamically integrate functions of many transcription regulators to induce spatiotemporal alterations in chromatin state and structure. Changes in gene expressions result in cell-specific responses that include proliferation, differentiation and death. Deregulation of E2-ER alpha signaling contributes to the initiation and progression of target tissue malignancies. We aim here to provide a review of recent findings on dynamic transcriptional events mediated by E2-ER alpha with the anticipation that a better understanding of complex regulatory mechanisms underlying ER actions would be a critical basis for the development of effective prognostic tools for and therapeutic interventions against estrogen target tissue malignancies.