SummaryBCL-2 molecules are regulators of programmed cell death Defects in this pathway contribute to human diseases. One family member, MCL-1, is unique because its expression is tightly regulated and it is essential for promoting the survival of a myriad of cellular lineages. Additionally, MCL-1 promotes the maintenance of normal mitochondrial morphology and energy production. Dissection of these functions revealed recently that they depend on separate mitochondrial sublocalizations. MCL-1's antiapoptotic activity is restricted to the outer mitochondrial membrane (OMM), whereas its function in mitochondrial physiology requires localization to the matrix. These findings provide an attractive model for how MCL-1's diverse functions may contribute to normal cell homeostasis and function. MCL-1 is highly amplified in human cancer, suggesting that these functions may contribute to malignant cell growth and evasion of apoptosis.
Keywordsapoptosis; MCL-1; homeostasis; mitochondrial function; cancer; development
THIS IS A SUMMARY OF AN ARTICLE FROM "TRENDS IN CELL BIOLOGY".
FOR MORE INFORMATION, PLEASE GO TO THE SOURCE.
WE ARE TRACKING SUPPORTIVE MATERIAL THAT REENFORCES OUR ASSUMPTIONS!
OUR ASSUMPTIONS STILL ARE THAT MEDICATIONS THAT AFFECT THE ACTINIC SCAFFOLDING (MICROTUBULE/MICROFILAMENT) BYPASS THE Bcl-2 RESISTANCE.
HOW MUCH AUTOPHAGY PLAYS INTO THIS IS STILL TO BE DETERMINED. AUTOPHAGY IS MEANT TO BE FOR CANCER SURVIVAL GLOBALLY AS A RESPONSE TO STRESS ON THE CANCER CELL. BUT THERE COMES A POINT WHEN IT IS DETRIMENTAL AND LEADS TO NON CASPASE CELL DEATH. OTHERS HAVE CALLED THIS (RIGHT OR WRONGLY) "NECROSIS".