Elimination of Mcl-1 is required for the initiation of apoptosis following ultraviolet irradiation
AUTOR(ES)
Nijhawan, Deepak
FONTE
Cold Spring Harbor Laboratory Press
RESUMO
Ultraviolet (UV) irradiation of HeLa cells triggers an apoptotic response mediated by mitochondria. Biochemical analysis of this response revealed that the elimination of cytosolic inhibitors is required for mitochondrial release of cytochrome c and subsequent caspase activation. These inhibitors were found to be Mcl-1 and Bcl-xL, two antiapoptotic members of the Bcl-2 family. Following UV treatment, Mcl-1 protein synthesis is blocked, the existing pool of Mcl-1 protein is rapidly degraded by the proteasome, and cytosolic Bcl-xL translocates to the mitochondria. These events are sequential; the elimination of Mcl-1 is required for the translocation of Bcl-xL. The disappearance of Mcl-1 is also required for other mitochondrial apoptotic events including Bax translocation, cytochrome c release, and caspase activation.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=196078Documentos Relacionados
- DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cells
- Mcl-1 Degradation during Hepatocyte Lipoapoptosis*
- Dynamic changes in Mcl-1 expression regulate macrophage viability or commitment to apoptosis during bacterial clearance
- Inhibition of STAT3 signaling leads to apoptosis of leukemic large granular lymphocytes and decreased Mcl-1 expression
- Mcl-1 deficiency results in peri-implantation embryonic lethality