1,2-Dibromoethane


Curated chemical-gene interactions from CTD
Entrez gene IDGene symbolInteraction typeReference
1066 CES1 Increases expression PMID:17311802
10732 TCFL5 Increases expression PMID:15612046
116285 ACSM1 Increases expression PMID:17311802
151242 PPP1R1C Decreases expression PMID:15612046
16061 IGH-VJ558 Increases expression PMID:22434383
1728 NQO1 Increases expression PMID:17311802
1820 ARID3A Increases expression PMID:15612046
1893 ECM1 Decreases expression PMID:15612046
2052 EPHX1 Decreases expression PMID:17311802
22061 TRP63 Increases expression PMID:15612046
23646 PLD3 Increases expression PMID:15612046
2678 GGT1 Increases activity PMID:12628311
2952 GSTT1 Increases activity PMID:12505322; PMID:19664997
3858 KRT10 Decreases expression PMID:22434383
4255 MGMT Decreases activity PMID:12151404
4780 NFE2L2 Increases activity PMID:30114225; PMID:30203046
4953 ODC1 Increases activity PMID:3801022
51176 LEF1 Decreases expression PMID:15612046
51393 TRPV2 Increases expression PMID:15612046
53834 FGFRL1 Decreases expression PMID:22434383
54879 ST7L Decreases expression PMID:15612046
5602 MAPK10 Increases expression PMID:15612046
56288 PARD3 Increases expression PMID:22434383
56852 RAD18 Decreases expression PMID:22434383
7166 TPH1 Increases expression PMID:15612046
9368 NHERF1 Increases expression PMID:22434383
9569 GTF2IRD1 Decreases expression PMID:22434383

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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.