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 |