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Mitochondria and cell death: outer membrane permeabilization and beyond
  • S. Tait, D. Green
  • Biology, Medicine
  • Nature Reviews Molecular Cell Biology
  • 1 September 2010
TLDR
MOMP typically leads to cell death irrespective of caspase activity by causing a progressive decline in mitochondrial function, although cells can survive this under certain circumstances, which may have pathophysiological consequences. Expand
The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis
TLDR
In a cell-free apoptosis system, mitochondria spontaneously released cytochrome c, which activated DEVD-specific caspases, leading to fodrin cleavage and apoptotic nuclear morphology, and Bcl-2 acts to inhibit cy tochrome c translocation, thereby blocking caspase activation and the apoptotic process. Expand
The Pathophysiology of Mitochondrial Cell Death
TLDR
The therapeutic induction of MOMP may restore apoptosis in cancer cells in which it is disabled, and the general rules governing the pathophysiology and controversial issues regarding its regulation are discussed. Expand
Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis
TLDR
It is proposed that when p53 accumulates in the cytosol, it can function analogously to the BH3-only subset of proapoptotic Bcl-2proteins to activate Bax and trigger apoptosis. Expand
Mitochondria and apoptosis.
A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembraneExpand
BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly.
TLDR
A unified model of BH3 domain function is supported, encompassing both positive and negative regulation of other Bcl-2 family members, and the simple inhibition of antiapoptotic functions is insufficient to induce apoptosis unless a direct activator of Bax or Bak is present. Expand
The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation.
TLDR
Metabolic tracer analysis revealed a Myc-dependent metabolic pathway linking glutaminolysis to the biosynthesis of polyamines, which may represent a general mechanism for metabolic reprogramming under patho-physiological conditions. Expand
Toll-like receptor signalling in macrophages links the autophagy pathway to phagocytosis
TLDR
It is shown that a particle that engages TLRs on a murine macrophage while it is phagocytosed triggers the autophagosome marker LC3 to be rapidly recruited to the phagosome in a manner that depends on theAutophagy pathway proteins ATG5 and ATG7; this process is preceded by recruitment of beclin 1 and phosphoinositide-3-OH kinase activity. Expand
The BCL-2 family reunion.
TLDR
The mechanisms and functions of the BCL-2 family are discussed in the context of these pathways, highlighting the complex integration and regulation of the b cell CLL/lymphoma-2family in cell fate decisions. Expand
Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012
TLDR
A functional classification of cell death subroutines is proposed that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic programmed cell death, regulated necrosis, autophagic cell death and mitotic catastrophe. Expand
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