Authors: Rhonda M. Perciavalle, Joseph T. Opferman
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Summary
BCL-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.Keywords
apoptosis; MCL-1; homeostasis; mitochondrial function; cancer; developmentTHIS IS A SUMMARY OF AN ARTICLE FROM "TRENDS IN CELL BIOLOGY".
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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".
