The translation initiation factor DAP5 is a regulator of cell survival during mitosis.
Initiation of protein translation is tightly regulated by various physiological signals and involves cap-dependent and independent mechanisms. DAP5 protein is an eIF4G family member previously implicated in mediating cap-independent IRES driven translation in response to various cellular stresses. Unexpectedly, we have recently found that DAP5 is also essential for continuous cell survival in non-stressed cells. We reported in this respect that the knock down of endogenous DAP5 by RNA-interference induces M-phase specific caspase-dependent cell death. Bcl-2 and CDK1 were identified as DAP5 mRNA targets, the translation of which was selectively reduced in the DAP5 knock down cells. They each possess a functional IRES element in their 5'UTR. Here we review the major results of this study and present new data on the link of DAP5 to additional Bcl-2 family members. In addition we discuss other possible cellular phenotypes resulting from the knock down of DAP5 in these cells.
Liberman
Noa
N
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Marash
Lea
L
Kimchi
Adi
A
D016203:CDC2 Protein Kinase / Q000378:metabolism; D002470:Cell Survival / Q000235:genetics / Q000502:physiology; D039603:Eukaryotic Initiation Factor-4G / Q000378:metabolism*; D006367:HeLa Cells; D006801:Humans; D008938:Mitosis; D010442:Peptide Chain Initiation, Translational / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism
C491300:EIF4G2 protein, human; D039603:Eukaryotic Initiation Factor-4G; D019253:Proto-Oncogene Proteins c-bcl-2; D016203:CDC2 Protein Kinase