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Table 2 DEGs in WT and MyTrMaSt mice

From: Mice defective in interferon signaling help distinguish between primary and secondary pathological pathways in a mouse model of neuronal forms of Gaucher disease

Gene WT + CBE versus WT + PBS MyTrMaSt + CBE versus MyTrMaSt + PB  
  Fold-change Fold-change  
Cholesterol metabolism
Dhcr24  3.34 − 1.67  
Mvd  2.60 − 1.27  
S1pr3 12.0 4.20  
Lipoprotein metabolism
Apobec1 13.0 3.63  
Apobec3 6.70 2.50  
Pon3 7.34 3.30  
Metalloproteinases
Aspg 22.2 8.50  
Mmp19 9.80 4.20  
Timp1 60.4 13.9  
Lysosome
Ctsc 8.60 2.60  
Ctss 6.60 2.90  
Inflammation (chemokines)
A2m 17.3 7.41  
Ccl2 161 14.1  
Ccl5 29.3 − 1.02  
Ccl12 39.6 8.80  
Cxcl1 42.2 16.1  
Cxcl10 77.7 3.06  
Cxcl16 12.6 3.38  
Ptprc 12.4 2.40  
Inflammation (TNF)
Ptx3 92.2 8.04  
Steap4 51.4 3.90  
Tnfaip2 40.6 4.07  
Inflammation (TGF)
Gdf15 59.9 4.80  
Tgfbi 9.63 2.05  
Inflammation (Microglia)
Cd300lf 42.3 11.4  
Lgals3bp 13.9 4.35  
Mac2 60.1 21.8  
P2ry6 7.96 3.96  
Complement
C31 32.1 3.01  
C3ar1 80.6 5.60  
Itgb2 14.7 5.78  
Others
Cst7 102 37.9  
Serpina3n 57.8 17.1  
Cd5l 32.6 7.9  
  1. A selection of the 90 DEGs whose levels were reduced > 2-fold in MyTrMaSt mice compared with WT mice, but were nevertheless still DE between MyTrMaSt + CBE versus MyTrMaSt + PBS. Fold-changes were all statistically significant (p < 0.01) except for the values in italics
  2. n.s. not significant
  3. 1 Validated by PCR: WT + CBE versus WT + PBS, fold-change 80.7 ± 16.2 (C3). MyTrMaSt + CBE versus MyTrMaSt + PBS, fold-change 21.2 ± 8.6