Fig. 1.

Experimental design. Wildtype (WT) C57BL/6J mice and Cyp1b1^−/− (Cyp1b1-null) mice were exposed for 48 h to either room air (RA) or hyperoxia (O₂). Lungs were collected and assayed for gene expression using microarray or for protein expression using Reverse Phase Protein Array (RPPA) platforms. We evaluated the transcriptional phenotype of Cyp1b1-null mice using gene signatures, enriched pathways, gene signature correlations, and clinical associations with potential lung disease endpoints.