Ziram


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0004030 Aldehyde dehydrogenase [nad(p)+] activity Decreases phenotype PMID:24491970
GO:0006006 Glucose metabolic process Affects phenotype PMID:32745781
GO:0006083 Acetate metabolic process Affects phenotype PMID:32745781
GO:0006105 Succinate metabolic process Affects phenotype PMID:32745781
GO:0006631 Fatty acid metabolic process Affects phenotype PMID:32745781
GO:0006735 Nadh regeneration Increases phenotype PMID:26859423
GO:0006882 Cellular zinc ion homeostasis Affects phenotype PMID:26026913
GO:0006909 Phagocytosis Affects phenotype PMID:32712770
GO:0006915 Apoptotic process Increases phenotype PMID:30422632; PMID:32712770
GO:0007224 Smoothened signaling pathway Decreases phenotype PMID:31652400
GO:0008203 Cholesterol metabolic process Affects phenotype PMID:32745781
GO:0008283 Cell population proliferation Increases phenotype PMID:29627606; PMID:32736067
GO:0010942 Positive regulation of cell death Increases phenotype PMID:25284465
GO:0018158 Protein oxidation Increases phenotype PMID:25714994
GO:0019627 Urea metabolic process Affects phenotype PMID:32745781
GO:0031987 Locomotion involved in locomotory behavior Decreases phenotype PMID:32736067
GO:0033327 Leydig cell differentiation Decreases phenotype PMID:28973382
GO:0035176 Social behavior Affects phenotype PMID:32736067
GO:0035936 Testosterone secretion Decreases phenotype PMID:28973382; PMID:29627606
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:26026913; PMID:28973382
GO:0043525 Positive regulation of neuron apoptotic process Increases phenotype PMID:12782107
GO:0044237 Cellular metabolic process Decreases phenotype PMID:32712770; PMID:32870474
GO:0046882 Negative regulation of follicle-stimulating hormone secretion Increases phenotype PMID:28973382
GO:0048384 Retinoic acid receptor signaling pathway Decreases phenotype PMID:31652400
GO:0050872 White fat cell differentiation Increases phenotype PMID:32745781
GO:0051480 Regulation of cytosolic calcium ion concentration Affects phenotype PMID:25284465
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:25284465; PMID:30422632
GO:0060070 Canonical wnt signaling pathway Decreases phenotype PMID:31652400
GO:0061370 Testosterone biosynthetic process Decreases phenotype PMID:30422632
GO:0070265 Necrotic cell death Increases phenotype PMID:32712770
GO:0070995 Nadph oxidation Increases phenotype PMID:26859423
GO:0071578 Zinc ion import across plasma membrane Increases phenotype PMID:25714994; PMID:26026913
GO:0071629 Cytoplasm protein quality control by the ubiquitin-proteasome system Decreases phenotype PMID:23988235
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:32712770
GO:0098705 Copper ion import across plasma membrane Increases phenotype PMID:25714994
GO:1901216 Positive regulation of neuron death Increases phenotype PMID:25284465
GO:1902656 Calcium ion import into cytosol Increases phenotype PMID:12782107; PMID:25284465
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:30422632
GO:1990138 Neuron projection extension Decreases phenotype PMID:31652400
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.