Transient protection by peripheral benzodiazepine receptors during the early events of ultraviolet light-induced apoptosis. (scientific article published in July 2001)

Cleavage of BID during cytotoxic drug and UV radiation-induced apoptosis occurs downstream of the point of Bcl-2 action and is catalysed by caspase-3: a potential feedback loop for amplification of apoptosis-associated mitochondrial cytochrome c rel

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The expression of peripheral benzodiazepine receptors in human skin: the relationship with epidermal cell differentiation

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Caspase-3-dependent cleavage of Bcl-2 promotes release of cytochrome c

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Cloning and characterization of PRAX-1. A new protein that specifically interacts with the peripheral benzodiazepine receptor

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Mitochondrio-nuclear translocation of AIF in apoptosis and necrosis

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Emerging roles of caspase-3 in apoptosis

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Benzodiazepine receptor agonists modulate thymocyte apoptosis through reduction of the mitochondrial transmembrane potential

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Mitochondria and apoptosis

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Ultraviolet light induces apoptosis via direct activation of CD95 (Fas/APO-1) independently of its ligand CD95L

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Suicidal tendencies: apoptotic cell death by caspase family proteinases

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Light and death: photons and apoptosis

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Distinct stages of cytochrome c release from mitochondria: evidence for a feedback amplification loop linking caspase activation to mitochondrial dysfunction in genotoxic stress induced apoptosis

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Porphyrins are endogenous ligands for the mitochondrial (peripheral-type) benzodiazepine receptor

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Specific benzodiazepine receptors in rat brain characterized by high-affinity (3H)diazepam binding

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Tumor selective G2/M cell cycle arrest and apoptosis of epithelial and hematological malignancies by BBL22, a benzazepine

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Adenine nucleotide translocase-1, a component of the permeability transition pore, can dominantly induce apoptosis

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Reduction in mitochondrial potential constitutes an early irreversible step of programmed lymphocyte death in vivo.

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Sequential reduction of mitochondrial transmembrane potential and generation of reactive oxygen species in early programmed cell death

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Mitochondrial control of nuclear apoptosis.

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Mitochondrial permeability transition is a central coordinating event of apoptosis

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The permeability transition pore complex: a target for apoptosis regulation by caspases and bcl-2-related proteins

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Peripheral benzodiazepine receptor agonists exhibit potent antiapoptotic activities

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Molecular and functional properties of mitochondrial benzodiazepine receptors

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Activation of p38 mitogen-activated protein kinase and caspases in UVB-induced apoptosis of human keratinocyte HaCaT cells

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Mitochondrial control of apoptosis

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The proto-oncogene Bcl-2 and its role in regulating apoptosis

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Caspases induce cytochrome c release from mitochondria by activating cytosolic factors

Q41671448

Caspase-3 is the primary activator of apoptotic DNA fragmentation via DNA fragmentation factor-45/inhibitor of caspase-activated DNase inactivation.

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The coordinate release of cytochrome c during apoptosis is rapid, complete and kinetically invariant

Q41723645

Role of ultraviolet A-induced oxidative DNA damage in apoptosis via loss of mitochondrial membrane potential and caspase-3 activation

Q47907259

PK11195, a ligand of the mitochondrial benzodiazepine receptor, facilitates the induction of apoptosis and reverses Bcl-2-mediated cytoprotection.

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TspO of rhodobacter sphaeroides. A structural and functional model for the mammalian peripheral benzodiazepine receptor

Q73462971

P433

issue

P304

page(s)

747-753

P577

publication date

2001-07-01

P1433

published in

Cell Death & Differentiation

Q2943974

P1476

title

Transient protection by peripheral benzodiazepine receptors during the early events of ultraviolet light-induced apoptosis

P478

volume

Reverse relations

cites work (P2860)

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