Uzen Savas

TL;DR: CYP1B1-null mice, created by targeted gene disruption in embryonic stem cells, were born at the expected frequency from heterozygous matings with no observable phenotype as discussed by the authors.

TL;DR: Hybridization of mRNA and immunoblot analyses of microsomes both demonstrated beta-naphthoflavone (beta-NF) inducibility of Cyp1b-1 expression in C3H mouse lung, liver, and uterus although at lower levels relative to Cyp1a-1.

TL;DR: The atomic structure of human P450 1B1 was determined by x-ray crystallography to 2.7 Å resolution with α-naphthoflavone bound in the active site cavity with sequence divergence around the edges of the cavity that modify substrate and inhibitor binding.

TL;DR: The key role of the AhR is demonstrated in constitutive as well as TCDD-induced expression of Cyp1B1in mouse embryo fibroblasts and oligonucleotides that encompass two other XREs show a high affinity complex of similar size that is evident even without T CDD treatment and that does not contain either the Ahr or AhR nuclear translocator.

TL;DR: Each P450 exhibits a surprisingly similar pattern of hormonal regulation even though expressed in different cell types, suggesting that this arises from exceptionally active CYP1B1 in a small proportion (5%) of residual RMF.