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. Author manuscript; available in PMC: 2013 May 16.
Published in final edited form as: Toxicology. 2012 Feb 21;295(1-3):56–67. doi: 10.1016/j.tox.2012.01.017

Table 3A.

KEGG molecular pathway enrichment analysis of gene expression changes from control P53 versus 1200 μg/kg BW B(a)P-exposed offspring heart tissue transcriptome data set.

KEGG enriched pathway Observed [O] Expected [E] Enrichment [R] = [O]/[E] Raw p-value BH adjusted p-value
PPAR signaling pathway 6 0.40 14.88 3.31E–06 1.00E–04
Renin-angiotensin system 2 0.11 18.35 5.30E–03 2.13E–02
Hematopoietic cell lineage 5 0.42 11.91 6.58E–05 1.10E–03
Drug metabolism by CYPP450 4 0.45 8.84 1.10E–03 9.40E–03
Tight junction 5 0.73 6.85 9.00E–04 9.40E–03
Cell adhesion molecules-CAMs 5 0.86 5.84 1.70E–03 1.16E–02
Primary bile acid biosynthesis 2 0.08 24.46 3.00E–03 1.70E–02
Retinol metabolism 3 0.38 7.98 6.40E–03 2.13E–02
Metabolism of xenobiotics by CYPP450 3 0.39 7.75 6.90E–03 2.13E–02

Enrichment analysis from control P 53 versus 1200 μg/kg BW transcriptome data set. Column 1 – Significantly enriched KEGG pathway. Column 2 – Enrichment ratio (R) derived by ratio of significantly altered genes mapping to the pathway versus expected number of genes mapping to pathway form a reference baseline database. Column 3 – raw enrichment p-value of hypergeometic test for enrichment. Column 4 – Benjamini and Hochburg adjusted p-value to correct for multiple testing.