Title : Development of an adverse outcome pathway for cranio-facial malformations: A contribution from in silico simulations and in vitro data.

Pub. Date : 2020 Jun

PMID : 32251704






3 Functional Relationships(s)
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1 The proposed MIE for azole fungicides is CYP26 inhibition with retinoic acid (RA) local increase, triggering key events leading to craniofacial defects. Tretinoin cytochrome P450 family 26 subfamily A member 1 Homo sapiens
2 The proposed MIE for azole fungicides is CYP26 inhibition with retinoic acid (RA) local increase, triggering key events leading to craniofacial defects. Tretinoin cytochrome P450 family 26 subfamily A member 1 Homo sapiens
3 Unexpectedly, VPA showed also a weak, but not marginal, capability to enter the CYP 26A1 and CYP 26C1 catalytic sites, suggesting a possible role of VPA in decreasing RA catabolism, acting as an additional MIE. Tretinoin cytochrome P450 family 26 subfamily A member 1 Homo sapiens