Estrogen receptor alpha (ERalpha) is a ligand-dependent transcription factor that directs the transcription of a wide number of estrogen-regulated genes. ERalpha mediates the effects of 17-beta-estradiol in both males and females, and was the first estrogen receptor identified. Despite the cloning of the mouse ERalpha cDNA over 15 years ago, the precise genomic organization of the mouse ERalpha gene has not yet been elucidated. In order to determine the structure of this gene, overlapping BAC and P1 clones containing partial genomic sequences of the mouse ERalpha cDNA were obtained from a mouse ES cell genomic library. Using standard restriction fragment analysis followed by Southern blotting, the mouse ERalpha gene was determined to be greater than 220 kb in length. The introns vary widely in size, from 1.8 to 60 kb in length. Sequencing of intron-exon boundaries shows that these boundaries are highly conserved between the human and mouse ERalpha genes. Additionally, we have identified a splice variant message of mouse ERalpha arising from a failure to properly splice at the 3' end of exon 4; the resulting message is predicted to produce a protein lacking the ligand-binding domain. Variant message was detected by RT-PCR in several tissues, including uterus, ovary, mammary gland, placenta and testis.
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http://dx.doi.org/10.1016/s0378-1119(02)00796-5 | DOI Listing |
Breast Cancer Res
January 2025
Division of Medical Oncology, The Ohio State University Comprehensive Cancer Center, Columbus, OH, USA.
Background: Epidemiological studies associate an increase in breast cancer risk, particularly triple-negative breast cancer (TNBC), with lack of breastfeeding. This is more prevalent in African American women, with significantly lower rate of breastfeeding compared to Caucasian women. Prolonged breastfeeding leads to gradual involution (GI), whereas short-term or lack of breastfeeding leads to abrupt involution (AI) of the breast.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Background: Estrogens, such as 17β-estradiol, are the primary female sex hormones predominantly synthesized by mature ovarian follicular cells. The natural exhaustion of ovarian follicular cells during menopause causes a rapid decline in endogenous estrogen levels. This decline in estrogen levels is associated with an increase in chronic, age-related pathologies, including inflammation in the brain.
View Article and Find Full Text PDFJ Med Chem
January 2025
Key laboratory of Plant Resource Conservation and Germplasm Innovation in Mountainous Region (Ministry of Education), Guizhou Engineering Laboratory for Synthetic Drugs, School of Pharmaceutical Sciences, Guizhou University, Guiyang 550025, PR China.
The relentless pursuit of innovative hydrophobic tags remains a formidable challenge within the realm of targeted protein degradation. Herein, we have uncovered the remarkable potential of D-ring-contracted artemisinin as a potent hydrophobic tag that demonstrates exceptional degradation efficiency. We have crafted a series of conjugates by fusing D-ring-contracted artemisinin with raloxifene, and among these, has emerged as a promising candidate for degrading estrogen receptor α (ERα).
View Article and Find Full Text PDFMetabolism
December 2024
Translational Nuclear Receptor Research, UGent Department of Biomolecular Medicine, VIB Center for Medical Biotechnology, Ghent, Belgium. Electronic address:
Background And Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD), the most prevalent liver disease worldwide, continues to rise. More effective therapeutic strategies are urgently needed. We investigated how targeting two key nuclear receptors involved in hepatic energy metabolism, peroxisome proliferator-activated receptor alpha (PPARα) and estrogen-related receptor alpha (ERRα), ameliorates MASLD.
View Article and Find Full Text PDFCell Rep Med
December 2024
Department of Surgery, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Atrium Health Wake Forest Baptist Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA. Electronic address:
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