Apoptosis is a mechanism of programmed cell death and is essential for development and homeostasis. Cell stress stimulates pro-apoptotic signalling pathways that activate caspase proteases and cause mitochondrial dysfunction. Apoptotic cells undergo characteristic changes in cell morphology, including cell rounding, plasma membrane blebbing and nuclear fragmentation.


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  • News and Views |

    During injury, mitogenic signals from apoptotic cells may compensate for cell loss by promoting organ homeostasis and regeneration. A distinct type of early apoptotic extracellular vesicle with specific mitogenic activity has been identified. The detection of these vesicles in damaged mouse glomeruli highlights their possible role in response to renal injury.

    • Benedetta Bussolati
    •  & Giovanni Camussi
  • News and Views |

    Effectiveness of EGFR treatment is impaired through an early adaptive response. TNF–JNK–Axl–ERK signaling contributes to this primary resistance to EGFR inhibition and might serve as novel target to improve EGFR inhibition.

    • Rolf Warta
    •  & Christel Herold-Mende
    Nature Neuroscience 20, 1035–1037
  • News and Views |

    Two new studies show that RNA-binding proteins can mediate distinct and beneficial effects to cells by binding to the extensive double-stranded RNA (dsRNA) structures of inverted-repeat Alu elements (IRAlus). One study reports stress-induced export of the 110-kDa isoform of the adenosine deaminase acting on RNA 1 protein (ADAR1p110) to the cytoplasm, where it binds IRAlus so as to protect many mRNAs encoding anti-apoptotic proteins from degradation. The other study demonstrates that binding of the nuclear helicase DHX9 to IRAlus embedded within RNAs minimizes defects in RNA processing.

    • Reyad A Elbarbary
    •  & Lynne E Maquat
  • News and Views |

    Although the mitochondrial inner membrane rhomboid peptidase PARL is known to participate in critical signalling cascades, its role in apoptosis has remained unclear. PARL is now shown to process the mitochondrial pro-apoptotic protein Smac (also known as DIABLO) for its subsequent release into the cytosol where it antagonizes XIAP-mediated caspase inhibition to promote apoptosis.

    • Naotada Ishihara
    •  & Katsuyoshi Mihara
    Nature Cell Biology 19, 263–265