INTERACTION OF RECEPTOR INTERACTING PROTEIN 1 (RIP1) AND NUCLEOPHOSMIN IN THE REGULATION OF CELL DEATH

Abstract

NUCLEOPHOSMIN (NPM) IS A UBIQUITOUS PROTEIN THAT HAS NUMEROUS CELLULAR FUNCTIONS. A FRAME-SHIFT MUTATION AT ITS C-TERMINUS ALLOWS FOR THE CREATION OF ADDITIONAL NUCLEAR EXPORT SIGNAL (NES) MOTIF WHICH CAUSED AN ABERRANT LOCALIZATION OF NPM TO THE CYTOPLASM THAT ALTERS THE INTERACTION DYNAMICS OF NPM AND ITS INTERACTORS WITH RESPECT TO SPATIAL AND TEMPORAL KINETICS. IN PREVIOUS STUDY, CYTOPLASMIC RESIDING NUCLEOPHOSMIN (NPMC) IS SHOWN TO ABROGATE APOPTOSIS THROUGH ITS INTERACTION WITH CLEAVED CASPASE 8 AND CASPASE 6 IN ACUTE MYELOID LEUKAEMIA CELLS (AML) CELLS. HOWEVER, SEVERAL SCIENTIFIC STUDIES REPORTED THAT A COMPROMISED STATE OF APOPTOSIS RENDER CELLS THE UTILIZATION OF AN ALTERNATIVE (POSSIBLY RUDIMENTARY) CELL DEATH PATHWAY UPON TUMOUR-NECROSIS-FACTOR-RELATED-APOPTOSIS-INDUCING LIGAND (TRAIL) TREATMENT. OF LATE, THE STUDY OF ALTERNATIVE CELL DEATH PATHWAY IS GAINING TRACTION AS A POSSIBLE THERAPEUTIC ROUTE FOR APOPTOSIS INSENSITIVE CELLS.

THE EMERGENCE OF AN INDUCIBLE AND REGU