Table 1.
Predominantly Pro-Inflammatory Effects. (Due to Active GSK3) |
Predominantly Anti-Inflammatory Effects (Due to GSK3 Inhibition) |
---|---|
NF-κB DNA binding activity ↑ | NF-κB DNA binding activity ↓ |
NF-κB transactivation activity ↑ (pro-inflammatory genes) |
NF-κB transactivation activity ↓ (pro-inflammatory genes) |
p65 phosphorylation (Thr254, Ser276, Ser536) ↑ | p65 phosphorylation (Ser468) ↑ |
p105 phosphorylation (Ser903, Ser907)* ↑ | p105 stability ↑ |
p100 phosphorylation (Ser707)* ↑ | p100 stability ↑ |
NEMO phosphorylation (Ser8, Ser17, Ser31) ↑ | - |
RelB phosphorylation (Ser552)* ↑ | RelB stability ↑ |
Bcl-3 phosphorylation (Ser394, Ser398)* ↑ | Bcl-3 stability ↑ |
Jun/Fos phosphorylation ↑ | Jun/Fos phosphorylation ↓ |
AP-1 DNA binding activity ↓ | AP-1 DNA binding activity ↑ |
C/EBPβ-LIP DNA binding activity ↑ (anti-inflammatory genes) |
C/EBPβ-LAP DNA binding activity ↑ (anti-inflammatory genes) |
C/EBPβ transactivation activity ↓ (anti-inflammatory genes) |
C/EBPβ transactivation activity ↑ (anti-inflammatory genes) |
C/EBPβ phosphorylation (Thr188, Ser184, Ser179) ↑ |
C/EBPβ phosphorylation (Thr188, Ser184, Ser179) ↓ |
CREB activity ↓ | CREB activity ↑ |
* leads to subsequent degradation. ↑, increased; ↓, decreased.