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. Author manuscript; available in PMC: 2020 Jun 25.
Published in final edited form as: Toxicology. 2009 Oct 12;266(1-3):6–15. doi: 10.1016/j.tox.2009.10.004

Table 2.

IPA functional category analysis of genes whose expression response to arsenic at 1 year was significant for the continuous treatment regimen. Only the top 12 categories are shown for each division, in order of significance.

No. ofgenes
Molecular and cellular functions
 Cellular compromise 347
 Gene expression 769
 Cellular growth and proliferation 976
 Cell death 951
 Post-translational modification 481
 Protein synthesis 366
 Protein degradation 144
 Molecular transport 354
 Protein trafficking 135
 Cell cycle 448
 RNA post-transcriptional modification 123
 Cell morphology 438
Top canonical pathways
 Protein ubiquitination pathway 96
 NRF2-mediated oxidative stress response 88
 PI3/AIKT signaling 66
 Molecular mechanisms of cancer 142
 Purine metabolism 127
 PTEN signaling 53
 Integrin signaling 86
 Mitochondrial dysfunction 60
 Chronic myeloid leukemia signaling 50
 Germ cell-sertoli cell junction signaling 67
 Insulin receptor signaling 62
 B cell receptor signaling 67
Top Tox lists
 Oxidative stress response mediated by NRF2 89
 Mitochondrial dysfunction 58
 Hypoxia-inducible factor signaling 40
 PPARa/RXR activation 73
 Mechanism ofgene regulation by peroxisome proliferaters via PPARa 48
 Hepatic cholestasis 58
 NFkB signaling 51
 RAR activation 58
 PXR/RXR activation 29
 P53 signaling 36
 Aryl hydrocarbon receptor signaling 54
 FXR/RXR activation 34