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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