| abstract |
The activity of NF-kB is modulated through the effects of GSK-3 on NK-kB activity. Inhibition or down-regulation of GSK-3 results in decreased NF-kB activity. Inappropriate activation of NF-kB has been linked to inflammation and hyperproliferative disorders. Development of modulatory strategies provi de a novel therapeutic tool for the treatment or prevention of various diseases . Methods are also provided for enhanced killing of tumor cells through the sensitization action of GSK-3 inhibition, when administered in conjunction with apoptosis inducing ligands of TNFR1. Transgenic animals defective in GS K- 3 function are also provided. |