Estrogen receptor pathways to AP-1.

By P. Kushner, David A. Agard, G. Greene, T. Scanlan, A. Shiau, R. Uht, P. Webb. Journal of Steroid Biochemistry and Molecular Biology, 2000

949 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/35574c5bc7cefed6ebd67a6d370026c131e14c53

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. Jason S. Carroll
2. Carolyn L. Smith
3. B. O’Malley
4. Mitchell Dowsett
5. G. Gillies
6. Myles A. Brown
7. X. S. Liu
8. S. McArthur

In Molecular Biology

1. X. S. Liu
2. Clifford A. Meyer
3. Myles A. Brown
4. Jason S. Carroll
5. B. O’Malley
6. Thomas R. Gingeras
7. Pamela A. Silver
8. Robert J. Handa

Citations in the corpus

• Principles for modulation of the nuclear receptor superfamily (2004, neutral): “fcgi?db=gene&cmd=Retrieve&dopt=Graphics&list_uids=3725">AP1”
• Hypothalamic–pituitary–adrenal and hypothalamic–pituitary–gonadal axes: sex differences in regulation of stress responsivity (2017, background): “These types of data suggest a potential interaction between these two molecules, where nuclear receptors may act to directly regulate gene transcription (Kushner et al., 2000; Lefstin & Yamamoto, 1998) such as CRH (Miller, Suzuki, Miller, Handa, & Uht, 2004).”
• Estrogen receptor β causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2 (2011, background): “We focused on these genes, because ERa binding sites have been identified in the BTG2 promoter [29] and both genes contain binding sites for AP1, which is known to be involved in ERa-mediated regulation of gene transcription [38, 39].”
• Mechanisms of tamoxifen resistance. (2004, background): “ERs can also regulate gene expression without interacting with DNA directly, via other transcription factors such as the Fos/Jun activating protein-1(AP-1) complex (non-classical mode) (Kushner et al. 2000, De Nardo et al. 2003, Schiff et al. 2003).”
• The matrix metalloproteinase system: changes, regulation, and impact throughout the ovarian and uterine reproductive cycle. (2003, background): “During periods of increasing estrogen exposure, the ligandbound estrogen receptor complex can increase expression of the transcription factors fos and jun (226, 227) that bind the activator protein-1 (AP-1) element.”
• The pros and cons of phytoestrogens (2010, positive): “Pelissero C, Lenczowski M, Chinzi D, Davail-Cuisset B, Sumpter J, Fostier A. Effects of flavonoids on aromatase activity, and in vitro study.”
• Estrogen signaling through the transmembrane G protein-coupled receptor GPR30. (2008, background): “Estrogen receptor α regulates matrix metalloproteinase-13 promoter activity primarily through the AP-1 transcriptional regulatory site.”
• ESR1 mutations as a mechanism for acquired endocrine resistance in breast cancer (2015, positive): “The ligand-independent activity of the ER mutants also conferred a cell-proliferation advantage to cells grown in oestrogen-deprived conditions or in the presence of fulvestrant and tamoxifen.38,41,42 Increased ligand- independent tumour growth was also observed in vivo using xenograft models of ER+”
• Genome-wide analysis of estrogen receptor binding sites (2006, background): “, and c-Jun has an extensively characterized role modulating estrogen target gene”
• Estrogen Actions in the Brain and the Basis for Differential Action in Men and Women: A Case for Sex-Specific Medicines (2010, background): “Specifically, estradiol can activate transcription via the activated protein-1 response element in the presence of ER but fails to do so when liganded with ER (Paech et al., 1997; Kushner et al., 2000).”
• Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer. (2004, background): “ER can also complex with other transcription factors, such as Fos and Jun proteins on AP1 response elements, to alter the transcription of genes not normally thought to be classical estrogen targets, such as cyclin D1, insulin-like growth factor 1, and collagenase ( 7 ).”
• Mechanisms of estrogen receptor signaling: convergence of genomic and nongenomic actions on target genes. (2005, background): “subtype and on the type of ligand (16).”