Molecular Determinants for the Tissue Specificity of SERMs

By Yongfeng Shang, Myles A. Brown. Science, 2002

1,184 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/298e13298514b672ff94ac8c485f3ea46ab9a0b5

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Citations in the corpus

Large effects from small exposures. I. Mechanisms for endocrine-disrupting chemicals with estrogenic activity. (2003, background): “There are also tissue-specific components of the transcriptional apparatus (receptor coregulators) involved in determining which genes are regulated by ligand-activated receptors (43,44).”
Genome-wide analysis of estrogen receptor binding sites (2006, background): “Estrogen receptor–mediated transcription has been intensively studied on a small number of endogenous target promoter”
Coregulator function: a key to understanding tissue specificity of selective receptor modulators. (2004, background): “ChIP experiments have demonstrated distinct patterns of tamoxifen-induced association of the promotors of the c-Myc and cathepsin D genes with coactivators and corepressors (146).”
Profiling of estrogen up- and down-regulated gene expression in human breast cancer cells: insights into gene networks and pathways underlying estrogenic control of proliferation and cell phenotype. (2003, background): “For example, the level of SRC1 in uterine cells is a critical determinant of how these cells respond to the SERM tamoxifen (12).”
The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. (2003, neutral): “, NCoR, SMRT, SRC-1, CBP) by means of RNAi (235, 460).”
LSD1 is a subunit of the NuRD complex and targets the metastasis programs in breast cancer. (2009, methodology): “LSD1 Is an Integral Component of the NuRD Complex Molecular carcinogenesis has been the primary research focus in this laboratory (Shang, 2006; Shang and Brown, 2002; Shang et al., 2000; Shi et al., 2007; Wu et al., 2005; Yin et al., 2004).”
Estrogen response element-dependent regulation of transcriptional activation of estrogen receptors α and β by coactivators and corepressors (2004, background): “Chromatin immunoprecipitation experiments revealed that NCoR interacts with ER in the promoters of the c-Myc and cathepsin D genes in MCF-7 breast cancer cells treated with tamoxifen or raloxifene (Shang & Brown 2002), indicating that these corepressors play a role in transcriptional silencing.”
The many faces of PPARgamma. (2005, neutral): “Of note, tissue-selective cofactor recruitment is also a hallmark of SERMs (Shang and Brown, 2002).”
Chromosome-wide mapping of estrogen receptor binding reveals long-range regulation requiring the forkhead protein FoxA1. (2005, background): “Significant progress has been made over the past decade in defining the complex interactions between chromatin and an array of factors involved in ER-mediated gene expression (Halachmi et al., 1994; Metivier et al., 2003; Shang and Brown, 2002; Shang et al., 2000), including the cyclic association o”
Principles for modulation of the nuclear receptor superfamily (2004, background): “Importantly, recent studies have shed light on the molecular mechanisms underlying SNuRM action, which has made it possible to design screening and target validatio”
Role of the estrogen receptor coactivator AIB1 (SRC-3) and HER-2/neu in tamoxifen resistance in breast cancer. (2003, background): “0–4 125 ( 41 ) 50 (44) 72 (40) 5–8 177 (59) 63 (56) 108 (60) .54 Missing 14 6 7”
Skeletal remodeling in health and disease (2007, background): “Designer estrogens bind to the same receptor in separate tissues to elicit different outputs by recruiting distinct co-regulator”
Overview of Nomenclature of Nuclear Receptors (2006, background): “…it has been shown that some antagonists significantly enhance this interaction, as well as HDAC recruitment, at certain ER (cid:1) target promoters (Jackson et al., 1997; Lavinsky et al., 1998; Zhang et al., 1998; Shang et al., 2000; Yamamoto et al., 2001; Shang and Brown, 2002; Webb et al., 2003).”
Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer. (2004, methodology): “... has estrogen agonist activity on estrogen target genes in MCF-7/HER2-18 cells, we next examined the assembly of ER transcription complex components on the well-characterized estrogen-responsive pS2 promoter by using ChIP assays (Fig. 4, C). We reasoned that, under conditions of enhanced EGFR and”
Molecular determinants of resistance to antiandrogen therapy (2004, background): “Previous work has shown that the agonist-versus-antagonist response of nuclear receptors, such as the estrogen receptor, is altered by increased expression of coactivators (such as SRC-1) or by decreased expression of corepressors (such as NCoR”