Furan


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000165 Mapk cascade Affects phenotype PMID:24183702
GO:0001541 Ovarian follicle development Affects phenotype PMID:32174189
GO:0003993 Acid phosphatase activity Decreases phenotype PMID:32758512
GO:0004035 Alkaline phosphatase activity Decreases phenotype PMID:32758512
GO:0004364 Glutathione transferase activity Decreases phenotype PMID:32758512
GO:0004457 Lactate dehydrogenase activity Decreases phenotype PMID:32758512
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:32758512
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:32758512; PMID:34450210
GO:0006006 Glucose metabolic process Affects phenotype PMID:27402187
GO:0006099 Tricarboxylic acid cycle Affects phenotype PMID:27402187
GO:0006121 Mitochondrial electron transport, succinate to ubiquinone Decreases phenotype PMID:27402187
GO:0006304 Dna modification Increases phenotype PMID:32544017
GO:0006521 Regulation of cellular amino acid metabolic process Affects phenotype PMID:27402187
GO:0006536 Glutamate metabolic process Affects phenotype PMID:34450210
GO:0006749 Glutathione metabolic process Affects phenotype PMID:32544017; PMID:32758512; PMID:34450210
GO:0006805 Xenobiotic metabolic process Affects phenotype PMID:32251705
GO:0006954 Inflammatory response Increases phenotype PMID:34450210
GO:0007033 Vacuole organization Increases phenotype PMID:32758512
GO:0007283 Spermatogenesis Decreases phenotype PMID:32174189; PMID:32758512; PMID:32758512
GO:0008210 Estrogen metabolic process Affects phenotype PMID:32174189
GO:0008219 Cell death Increases phenotype PMID:32544017
GO:0008283 Cell population proliferation Increases phenotype PMID:27143483
GO:0008284 Positive regulation of cell population proliferation Affects phenotype PMID:24183702
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:37488932
GO:0008584 Male gonad development Affects phenotype PMID:32174189
GO:0008614 Pyridoxine metabolic process Affects phenotype PMID:27402187
GO:0010940 Positive regulation of necrotic cell death Increases phenotype PMID:39171654
GO:0016042 Lipid catabolic process Affects phenotype PMID:32758512; PMID:34450210
GO:0016577 Histone demethylation Increases phenotype PMID:25539665
GO:0018158 Protein oxidation Increases phenotype PMID:32544017
GO:0022602 Ovulation cycle process Affects phenotype PMID:32174189
GO:0030104 Water homeostasis Affects phenotype PMID:27402187
GO:0030308 Negative regulation of cell growth Increases phenotype PMID:37488932
GO:0031098 Stress-activated protein kinase signaling cascade Affects phenotype PMID:24183702
GO:0032125 Micronucleus organization Increases phenotype PMID:37488932
GO:0032776 Dna methylation on cytosine Increases phenotype PMID:27371368
GO:0033209 Tumor necrosis factor-mediated signaling pathway Affects phenotype PMID:24183702
GO:0034720 Histone h3-k4 demethylation Increases phenotype PMID:25539665
GO:0034773 Histone h4-k20 trimethylation Decreases phenotype PMID:24614236
GO:0036124 Histone h3-k9 trimethylation Affects phenotype PMID:24614236; PMID:27371368
GO:0042453 Deoxyguanosine metabolic process Affects phenotype PMID:34450210
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:37488932
GO:0043970 Histone h3-k9 acetylation Decreases phenotype PMID:24614236; PMID:25539665
GO:0043974 Histone h3-k27 acetylation Decreases phenotype PMID:25539665
GO:0044030 Regulation of dna methylation Affects phenotype PMID:24614236
GO:0044237 Cellular metabolic process Decreases phenotype PMID:32544017; PMID:32758512
GO:0044849 Estrous cycle Affects phenotype PMID:32174189
GO:0045821 Positive regulation of glycolytic process Decreases phenotype PMID:27402187
GO:0045930 Negative regulation of mitotic cell cycle Increases phenotype PMID:26198647
GO:0046034 Atp metabolic process Affects phenotype PMID:32544017
GO:0046092 Deoxycytidine metabolic process Affects phenotype PMID:34450210
GO:0046209 Nitric oxide metabolic process Affects phenotype PMID:32758512
GO:0046951 Ketone body biosynthetic process Increases phenotype PMID:27402187
GO:0050729 Positive regulation of inflammatory response Increases phenotype PMID:39171654
GO:0061024 Membrane organization Affects phenotype PMID:27402187
GO:0061370 Testosterone biosynthetic process Affects phenotype PMID:32174189; PMID:32758512
GO:0070858 Negative regulation of bile acid biosynthetic process Increases phenotype PMID:38160780
GO:0090459 Cellular aspartate homeostasis Affects phenotype PMID:27402187
GO:0090461 Cellular glutamate homeostasis Affects phenotype PMID:27402187
GO:0090462 Cellular ornithine homeostasis Affects phenotype PMID:27402187
GO:0090463 Cellular lysine homeostasis Affects phenotype PMID:27402187
GO:0090465 Cellular arginine homeostasis Affects phenotype PMID:27402187
GO:0097009 Energy homeostasis Affects phenotype PMID:27402187
GO:0097043 Histone h3-k56 acetylation Decreases phenotype PMID:24614236; PMID:25539665
GO:0097237 Cellular response to toxic substance Affects phenotype PMID:24183702
GO:0097722 Sperm motility Decreases phenotype PMID:32758512
GO:0098532 Histone h3-k27 trimethylation Increases phenotype PMID:27371368
GO:0120189 Positive regulation of bile acid secretion Increases phenotype PMID:38160780
GO:1902231 Positive regulation of intrinsic apoptotic signaling pathway in response to dna damage Increases phenotype PMID:37488932
GO:1904251 Regulation of bile acid metabolic process Affects phenotype PMID:27402187
GO:2001020 Regulation of response to dna damage stimulus Affects phenotype PMID:37488932
GO:2001169 Regulation of atp biosynthetic process Affects phenotype PMID:27402187

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.