Diethylstilbestrol


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000089 Mitotic metaphase Affects phenotype PMID:36384894
GO:0003006 Developmental process involved in reproduction Affects phenotype PMID:37471692
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:33173981
GO:0006357 Regulation of transcription by rna polymerase ii Increases phenotype PMID:27478869
GO:0006701 Progesterone biosynthetic process Increases phenotype PMID:28970132
GO:0006703 Estrogen biosynthetic process Decreases phenotype PMID:28970132
GO:0006754 Atp biosynthetic process Decreases phenotype PMID:28849599
GO:0006805 Xenobiotic metabolic process Increases phenotype PMID:29162470
GO:0006811 Monoatomic ion transport Increases phenotype PMID:10991979
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:34748853
GO:0006914 Autophagy Increases phenotype PMID:30153466
GO:0006915 Apoptotic process Affects phenotype PMID:10556781; PMID:11000096; PMID:12477725; PMID:17901126
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:27601420; PMID:28315349
GO:0007049 Cell cycle Decreases phenotype PMID:11000096
GO:0007133 Meiotic anaphase i Increases phenotype PMID:29458137
GO:0007137 Meiotic metaphase ii Increases phenotype PMID:29458137
GO:0007283 Spermatogenesis Decreases phenotype PMID:15800398; PMID:20163289
GO:0007565 Female pregnancy Decreases phenotype PMID:37471692
GO:0007566 Embryo implantation Decreases phenotype PMID:25486513
GO:0008217 Regulation of blood pressure Decreases phenotype PMID:3180492
GO:0008283 Cell population proliferation Affects phenotype PMID:17599374; PMID:19654912; PMID:24062438; PMID:24213142; PMID:24213142; PMID:32088792; PMID:7588483
GO:0008284 Positive regulation of cell population proliferation Affects phenotype PMID:25486513; PMID:29783106; PMID:29783106; PMID:35307500
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:26385866; PMID:29990529; PMID:32949729
GO:0008584 Male gonad development Affects phenotype PMID:23314658
GO:0010424 Dna methylation on cytosine within a cg sequence Increases phenotype PMID:35605701
GO:0010669 Epithelial structure maintenance Decreases phenotype PMID:29699156
GO:0010942 Positive regulation of cell death Increases phenotype PMID:31566444
GO:0016049 Cell growth Decreases phenotype PMID:36277366
GO:0016571 Histone methylation Increases phenotype PMID:24533973
GO:0016573 Histone acetylation Increases phenotype PMID:24533973; PMID:25088689; PMID:25088689
GO:0019432 Triglyceride biosynthetic process Increases phenotype PMID:25111128
GO:0019953 Sexual reproduction Decreases phenotype PMID:37471692
GO:0030154 Cell differentiation Increases phenotype PMID:11297507; PMID:7588483
GO:0030194 Positive regulation of blood coagulation Increases phenotype PMID:2821645
GO:0030199 Collagen fibril organization Decreases phenotype PMID:20163289
GO:0030520 Intracellular estrogen receptor signaling pathway Increases phenotype PMID:36513145
GO:0032412 Regulation of monoatomic ion transmembrane transporter activity Decreases phenotype PMID:10991979
GO:0033146 Regulation of intracellular estrogen receptor signaling pathway Affects phenotype PMID:26865669
GO:0033148 Positive regulation of intracellular estrogen receptor signaling pathway Increases phenotype PMID:25575267
GO:0035847 Uterine epithelium development Increases phenotype PMID:25575267
GO:0042307 Positive regulation of protein import into nucleus Decreases phenotype PMID:24154490
GO:0042554 Superoxide anion generation Increases phenotype PMID:28315349
GO:0044237 Cellular metabolic process Decreases phenotype PMID:34748853; PMID:36277366; PMID:36621641
GO:0045333 Cellular respiration Decreases phenotype PMID:28849599
GO:0045600 Positive regulation of fat cell differentiation Decreases phenotype PMID:26944108
GO:0045931 Positive regulation of mitotic cell cycle Increases phenotype PMID:35307500
GO:0046034 Atp metabolic process Affects phenotype PMID:32949729
GO:0046466 Membrane lipid catabolic process Increases phenotype PMID:9303565
GO:0046620 Regulation of organ growth Decreases phenotype PMID:15800398
GO:0046621 Negative regulation of organ growth Increases phenotype PMID:29699156
GO:0048598 Embryonic morphogenesis Decreases phenotype PMID:26385866; PMID:29990529
GO:0048608 Reproductive structure development Affects phenotype PMID:37471692
GO:0048863 Stem cell differentiation Decreases phenotype PMID:31119342
GO:0051298 Centrosome duplication Increases phenotype PMID:36384894
GO:0051306 Mitotic sister chromatid separation Increases phenotype PMID:36384894
GO:0060068 Vagina development Affects phenotype PMID:33476676
GO:0060669 Embryonic placenta morphogenesis Affects phenotype PMID:22733484
GO:0072520 Seminiferous tubule development Affects phenotype PMID:33173981
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:20815788; PMID:34748853
GO:0080182 Histone h3-k4 trimethylation Increases phenotype PMID:25088689
GO:0097280 Histamine secretion mediated by immunoglobulin Affects phenotype PMID:6422997
GO:0160024 Leydig cell proliferation Increases phenotype PMID:23314658
GO:1902100 Negative regulation of metaphase/anaphase transition of cell cycle Increases phenotype PMID:37247809
GO:1903087 Mitotic spindle pole body duplication Affects phenotype PMID:36384894
GO:1903109 Positive regulation of mitochondrial transcription Increases phenotype PMID:29699156
GO:1903465 Positive regulation of mitotic cell cycle dna replication Increases phenotype PMID:25575267
GO:1904146 Positive regulation of meiotic cell cycle process involved in oocyte maturation Increases phenotype PMID:29458137
GO:2000224 Regulation of testosterone biosynthetic process Decreases phenotype PMID:23620786
GO:2000225 Negative regulation of testosterone biosynthetic process Increases phenotype PMID:23873838
DISCLAIMER

We have built a comprehensive resource which compiles potential endocrine disrupting chemicals (EDCs) based on the observed adverse effects or endocrine-mediated endpoints in published experiments on humans or rodents to support basic research. We are not responsible for any errors or omissions in the published research articles or supporting literature on potential EDCs compiled in this resource. Users are advised to exercise their own judgement on the weight of evidence for potential EDCs compiled in this resource. Importantly, our sole goal to build this resource on potential EDCs is to enable future basic research towards better understanding of the systems-level perturbations upon chemical exposure rather than influencing regulatory advice on chemical use.