Nongenotropic, sex-nonspecific signaling through the estrogen or androgen receptors: dissociation from transcriptional activity.

By S. Kousteni, T. Bellido, L. Plotkin, Charles A. O’Brien, D. Bodenner, Li Han, K. Han, G. DiGregorio, J. Katzenellenbogen, B. Katzenellenbogen and 4 more. Cell, 2001

1,239 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Genetics, Oncology

View Paper: https://www.semanticscholar.org/paper/fa56bc2d738ae32107d5f561343f64ed634b83aa

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. S. Manolagas
2. Stephen Honig
3. P. Rackoff

In Oncology

1. S. Manolagas
2. S. Khosla
3. R. Jilka
4. B. Riggs
5. S. Kousteni
6. L. Melton
7. John Calvin Reed
8. E. Levin

Citations in the corpus

• Androgen receptor in prostate cancer. (2004, background): “The tyrosine kinase activity of Src is normally autoinhibited by interaction between the tyrosine kinase domain and the Src homology 2 (SH2) and SH3 domains.”
• Integration of the extranuclear and nuclear actions of estrogen. (2005, background): “pool may be efficacious in these respects (25, 76), but we”
• Sex steroids and bone. (2002, background): “We have determined that the nongenotropic Src/Shc/ERK-mediated antiapoptotic effect of estrogens or androgens on osteoblasts and osteocytes is transmitted by the ER␣, ER␤, or the AR with similar efficiency, irrespective of whether the ligand is an estrogen or an androgen (Kousteni et al., 2001).”
• Apoptosis-based therapies (2002, background): “cgi?l=367">androgen receptors ) can reportedly activate PI3K in a ligand-dependent manner, thereby triggering the AKT pathway for apoptosis suppressio”
• Sex steroids and the construction and conservation of the adult skeleton. (2002, background): “(70) that both E and T regulate apoptosis in mature osteoblasts via a rapid nongenomic action.”
• Estrogen and the Skeleton (2012, positive): “At a molecular level, the effects of estrogen on reducing osteoblast apoptosis are due to activation of the Src/Shc/ ERK signaling pathway (49) and downregulation of JNK, which alters the activity of a number of transcription factors, including Elk-1, CCAAT enhancer binding protein-β (C/ EBPβ), cycl”
• From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “Last but not least, the view that stimulation of FasL is unlikely to be the mechanism by which estrogens promote osteoclast apoptosis is supported by the evidence that estrogens have an antiapoptotic effect on osteoblasts (142, 143, 164), although murine and human osteoblasts do undergo Fas-mediated”