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Substrate group 1—Metabolic: Overall Effect is anti-diabetic |
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GS | Increase glycogen synthesis and glucose disposal (anti-diabetic) |
Unknown | Turn off hepatic glucose output (anti-diabetic) |
CREB | Reduce glucagon action (anti-diabetic) |
IRS1 | Stabilise IRS1 protein and enhance insulin action (anti-diabetic) |
Inhibitor2 | Inhibit PP1 (not clear if beneficial) |
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Substrate group 2—Growth: Predicted effect would be oncogenic, except for effect on mdm2/p53 and PTEN |
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BCL3 | Stabilise BCL3 (increased oncogenic potential) |
c-jun | Induce c-jun activity (increased oncogenic potential) |
c-myc | Stabilize c-myc protein (increased oncogenic potential) |
Mcl-1 | Stabilise Mcl-1 (antiapoptotic) |
p130Rb | Increase p130Rb degradation (cell cycle progression) |
PTEN | Decrease PI3K signaling (decrease growth factor signaling) |
IRS1 | Stabilise IRS1 and enhance PI3K signaling (increase growth) |
HIF1a | Stabilize HIF1a (could induce cell growth) |
eIF2B | Enhance protein translation (aid cell growth) |
VDAC | Enhance VDAC interaction with mitochondria (antiapoptotic) |
CTPS | Enhance CTP production (aid cell growth) |
FAK | Increase FAK activity (enhance cell spreading and migration) |
Mdm2 | Stabilise p53 (tumour suppression) |
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Substrate group 3—Alzheimer’s disease: Conducive to reducing AD pathology |
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Tau | Reduce tangle formation (anti-AD?) |
APP | Reduce abeta production (anti-AD?) |
CRMP2 | Regulate axon outgrowth, reduce CRMP2 found in AD (anti-AD?) |
MARK2 | Reduce tau phosphorylation (anti-AD?) |
Calcipressin | Regulate calcineurin action (anti-AD?) |
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Substrate group 4—Wnt and Hh signaling: Enhanced effect on Wnt and Hh signaling |
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b-catenin | Induce b-catenin levels (induce wnt signaling) |
Axin | Reduce axin levels (induce wnt signaling) |
APC | Reduce APC b-catenin interaction (induce wnt signaling) |
Ci155 | Reduce proteolysis of Ci155 (enhanced Hh signaling) |
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Substrate group 5—Other possible detrimental effects: |
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MAP1B | Reduce MAP1B interaction with microtubules (Wnt7a resistance) |
MAP2C | Increase MAP2C interaction with microtubules (effect not clear) |
CLASP2 | Alteration of actin-microtubule interaction (effect not clear) |
Dynamin I | Reduced presynaptic ADBE (effect not clear) |
Ngn2 | Impaired motor neuron designation (developmental?) |
PC2 | Relocalise PC2 (enhance polycystic kidney disease) |
Myocardin | Enhance mycardin action (cardiac hypertrophy?) |
NFAT | Nuclear localization (compromise immune system?) |
Unknown | Suppress IL-1β, IL-6, TNF, IL-12 (compromise immune system?) |
Unknown | Induction of IL-10 (compromise immune system?) |
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