Loss Of Calreticulin Function Decreases NFKB Activity By Stabilizing IKB Protein

Abstract Background: Transcription factor NFKB is activated by several processes including inflammation, endoplasmic-reticulum (ER) stress, increased Akt signaling and enhanced proteasomal degradation. Calreticulin is an ER Ca2+ binding chaperone, which regulates many cellular processes. Previously, we have shown that loss of calreticulin function results in the activation of ER stress that is accompanied by a significant increase in the proteasome activity. These changes increase the resistance of calreticulin deficient cells to apoptosis. A role for calreticulin has also been described in the regulation of immune response. Objectives: To examine the role of calreticulin in the activation of NFKB signaling leading to enhanced resistance to apoptosis of these cells. Methods:: Wild type and calreticulin deficient cells were used for measurement of transcriptional activity of NFKB. Cells were co-transfected with of NFKB reporter and-gal reporter plasmids followed by reporter gene assays. Western blot analys...