Pyrazinamide


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0002253 Activation of immune response Increases phenotype PMID:27933861
GO:0002693 Positive regulation of cellular extravasation Increases phenotype PMID:22431067
GO:0004069 L-aspartate:2-oxoglutarate aminotransferase activity Increases phenotype PMID:28425350
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:27919644; PMID:28063906; PMID:36878459
GO:0006006 Glucose metabolic process Affects phenotype PMID:28425350
GO:0006101 Citrate metabolic process Affects phenotype PMID:28425350
GO:0006600 Creatine metabolic process Affects phenotype PMID:28425350
GO:0006749 Glutathione metabolic process Affects phenotype PMID:22431067; PMID:28425350; PMID:36878459
GO:0006750 Glutathione biosynthetic process Affects phenotype PMID:27919644; PMID:28063906
GO:0006915 Apoptotic process Increases phenotype PMID:28063906
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:27919644
GO:0007283 Spermatogenesis Decreases phenotype PMID:27919644
GO:0008206 Bile acid metabolic process Affects phenotype PMID:35835356
GO:0008283 Cell population proliferation Decreases phenotype PMID:28063906
GO:0008652 Amino acid biosynthetic process Affects phenotype PMID:28425350
GO:0009100 Glycoprotein metabolic process Affects phenotype PMID:28425350
GO:0010917 Negative regulation of mitochondrial membrane potential Increases phenotype PMID:27461009
GO:0016042 Lipid catabolic process Increases phenotype PMID:27919644; PMID:28063906; PMID:28425350
GO:0018158 Protein oxidation Increases phenotype PMID:28425350
GO:0019249 Lactate biosynthetic process Increases phenotype PMID:27461009
GO:0019432 Triglyceride biosynthetic process Increases phenotype PMID:27071702
GO:0019695 Choline metabolic process Affects phenotype PMID:28425350
GO:0032782 Bile acid secretion Increases phenotype PMID:22431067
GO:0034440 Lipid oxidation Increases phenotype PMID:22431067; PMID:36878459
GO:0040018 Positive regulation of multicellular organism growth Decreases phenotype PMID:22431067
GO:0042104 Positive regulation of activated t cell proliferation Increases phenotype PMID:27933861
GO:0042157 Lipoprotein metabolic process Affects phenotype PMID:28425350
GO:0042632 Cholesterol homeostasis Decreases phenotype PMID:22431067
GO:0043372 Positive regulation of cd4-positive, alpha-beta t cell differentiation Increases phenotype PMID:27933861
GO:0043378 Positive regulation of cd8-positive, alpha-beta t cell differentiation Increases phenotype PMID:27933861
GO:0044237 Cellular metabolic process Decreases phenotype PMID:35835356; PMID:36878459
GO:0045454 Cell redox homeostasis Decreases phenotype PMID:22431067
GO:0045930 Negative regulation of mitotic cell cycle Affects phenotype PMID:27919644
GO:0046541 Saliva secretion Increases phenotype PMID:27071702
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:28063906; PMID:36878459
GO:0055072 Iron ion homeostasis Affects phenotype PMID:36878459
GO:0061024 Membrane organization Decreases phenotype PMID:28063906
GO:0070265 Necrotic cell death Increases phenotype PMID:36878459
GO:0070328 Triglyceride homeostasis Decreases phenotype PMID:22431067
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:36878459
GO:0097195 Pilomotor reflex Increases phenotype PMID:27071702
GO:0140042 Lipid droplet formation Increases phenotype PMID:27071702; PMID:35835356; PMID:36878459
GO:1901526 Positive regulation of mitophagy Increases phenotype PMID:27461009
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:22431067
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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.