Iodoacetic acid


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001547 Antral ovarian follicle growth Decreases phenotype PMID:31693920
GO:0004365 Glyceraldehyde-3-phosphate dehydrogenase (nad+) (phosphorylating) activity Decreases phenotype PMID:21671678
GO:0006096 Glycolytic process Decreases phenotype PMID:25086087
GO:0006754 Atp biosynthetic process Decreases phenotype PMID:19923925
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:26327680
GO:0008219 Cell death Increases phenotype PMID:18624922
GO:0008283 Cell population proliferation Decreases phenotype PMID:25944804; PMID:26327680
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:30396169
GO:0009060 Aerobic respiration Increases phenotype PMID:25086087
GO:0030166 Proteoglycan biosynthetic process Affects phenotype PMID:26817025
GO:0030278 Regulation of ossification Affects phenotype PMID:26817025
GO:0030336 Negative regulation of cell migration Increases phenotype PMID:30396169
GO:0031987 Locomotion involved in locomotory behavior Affects phenotype PMID:29017758; PMID:36584762
GO:0035640 Exploration behavior Decreases phenotype PMID:30945071; PMID:36584762
GO:0035929 Steroid hormone secretion Affects phenotype PMID:31693920
GO:0035936 Testosterone secretion Decreases phenotype PMID:31693920
GO:0035938 Estradiol secretion Decreases phenotype PMID:31693920
GO:0035941 Androstenedione secretion Decreases phenotype PMID:31693920
GO:0042701 Progesterone secretion Increases phenotype PMID:31693920
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:25944804
GO:0045124 Regulation of bone resorption Affects phenotype PMID:26817025
GO:0046034 Atp metabolic process Affects phenotype PMID:31104297
GO:0048266 Behavioral response to pain Increases phenotype PMID:30945071
GO:0070265 Necrotic cell death Increases phenotype PMID:26817025
GO:0071674 Mononuclear cell migration Increases phenotype PMID:26817025
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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.