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Table 2 Pathway analysis using Tian's method identified ERα agonist-regulated pathways related to immunity/inflammation.

From: Estrogens regulate neuroinflammatory genes via estrogen receptors α and β in the frontal cortex of middle-aged female rats

rank pathway set size percent up average (NTk, NEk)
1 graft-versus-host disease 67 9 7.2
2 autoimmune thyroid disease 73 8 7.5
3 allograft rejection 68 9 7.8
4 cell adhesion molecules 189 18 8.0
5 retinol metabolism 64 11 9.5
6 type I diabetes mellitus 77 16 11.2
7 hematopoietic cell lineage 101 18 13.5
8 neuroactive ligand-receptor interaction 335 16 13.8
9 pantothenate and CoA biosynthesis 11 27 14.5
10 C and coagulation cascades 92 13 14.5
11 androgen and estrogen metabolism 33 15 16.5
12 Parkinson's disease 139 69 16.5
13 cytokine-cytokine receptor interaction 210 23 20.5
14 systemic lupus erythematosus 92 22 22.2
15 caffeine metabolism 10 10 25.5
16 metabolism of xenobiotics by cytochrome P450 48 15 26.2
17 ECM-receptor interaction 101 24 26.2
18 Jak-STAT signaling pathway 172 28 27.2
19 drug metabolism - other enzymes 38 24 27.5
20 basal cell carcinoma 68 21 29.0
  1. The analysis identified eight immune-related KEGG pathways (in bold) regulated by selective ERα agonist 16α-LE2. In the analysis, KEGG pathways were used as collaborator gene sets. Using the Tian's method [31], the relationship between gene sets and treatment is quantified by two statistics (T k and E k ) formulating the two hypotheses: i) the gene in a gene set shows the same pattern of associations with the treatment compared with the rest of the genes, ii) the gene set does not contain any genes whose expression levels are associated with the treatment, respectively. KEGG pathways were ranked by the mean of normalized statistics (NT k and NE k ). Set size is the number of genes, percent up is the number of up-regulated genes in the KEGG pathway. C, complement.