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. 2010 Nov 10;11:624. doi: 10.1186/1471-2164-11-624

Table 4.

Top five canonical pathways associated with each gene cluster following infestation with P. ovis

Temporal cluster* Canonical Pathway p-valueA
Cluster 1 p38 MAPK signalling 2.9E-05
IL12 signalling and production in macrophages 5.4E-05
IL10 signalling 6.9E-05
Aryl hydrocarbon receptor signalling 1.3E-04
PPAR signalling 2.9E-04
Cluster 2 IL10 signalling 1.2E-10
Production of nitric oxide and reactive oxygen species in macrophages 1.0E-09
Dendritic cell maturation 1.8E-09
TREM1 signalling 1.8E-09
NF-kB signalling 6.7E-09
Cluster 3 T helper cell differentiation 6.4E-08
IL10 signalling 3.7E-06
NF-kB signalling 1.6E-05
Acute phase response signalling 6.1E-05
TREM1 signalling 2.4E-04
Cluster 4 Interferon signalling 1.3E-05
Leukocyte extravasation signalling 2.9E-05
Antigen presentation pathway 3.9E-05
T helper cell differentiation 1.7E-04
CD28 signalling in T helper cells 1.9E-04
Cluster 6 Complement system 5.3E-12
Role of pattern recognition receptors in recognition of bacteria and viruses 2.9E-06
Acute phase response signalling 8.7E-05
Role of macrophages, fibroblasts and endothelial cells in RA# 1.0E-03
Wnt/beta-catenin signalling 2.3E-02
Cluster 7 Aryl hydrocarbon receptor signalling 3.5E-03
Antiproliferative role of somatostatin receptor 2 7.1E-03
CCR5 signalling in macrophages 3.8E-02
Integrin signalling 5.8E-02
IL1 signalling 7.7E-02
Cluster 8 Tight junction signalling 2.4E-03
BMP signalling pathway 2.3E-02
TGF beta signalling 2.8E-02
IL6 signalling 3.8E-02
Wnt/beta-catenin signalling 5.1E-02

Key - *Cluster 5 contained too few genes for effective analysis of canonical pathways. #Rheumatoid arthritis. Ap-value calculated using Fisher's exact test determining the probability that association between genes in the data set and canonical pathway is due to chance alone