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10.1016/j.molcel.2016.02.019

http://scihub22266oqcxt.onion/10.1016/j.molcel.2016.02.019
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C4806554!4806554!26942674
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suck abstract from ncbi


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pmid26942674      Mol+Cell 2016 ; 61 (5): 695-704
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  • Mitochondria ? judges and executioners of cell death sentences #MMPMID26942674
  • Bhola P; Letai A
  • Mol Cell 2016[Mar]; 61 (5): 695-704 PMID26942674show ga
  • Apoptosis is a form of programmed cell death that is critical for basic human development and physiology. One of the more important surprises in cell biology in the last two decades is the extent to which mitochondria represent a physical point of convergence for many apoptosis inducing signals in mammalian cells. Mitochondria not only adjudicate the decision of whether or not to commit to cell death, but also release toxic proteins culminating in widespread proteolysis, nucleolysis, and cell engulfment. Interactions among Bcl-2 family proteins at the mitochondrial outer membrane controls the release of these toxic proteins, and by extension control cellular commitment to apoptosis. This pathway is particularly relevant to cancer treatment, as most cancer chemotherapies trigger mitochondrial mediated apoptosis. In this review, we discuss recent advances in the Bcl-2 family interactions, their control by upstream factors, and how the mitochondria itself alters these interactions. We also highlight recent clinical insights into mitochondrial mediated apoptosis and novel cancer therapies that exploit this pathway.Introduction: Mitochondria adjudicate the cell death decision in response to many physiological and therapeutic stimuli. The review we highlight seminal and recent advances on how mitochondria and the Bcl-2 family of proteins regulate cell death. In particular we discuss recent advances in the Bcl-2 family interactions, their control by upstream factors, and how the mitochondria itself alters these interactions. We also highlight recent clinical insights into mitochondrial mediated apoptosis and how cancer therapies that exploit this pathway.
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