◀ Back to BCL2
BCL2 — DIABLO
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Adrain et al., EMBO J 2001
:
Thus, in addition to modulating apoptosis associated mitochondrial cytochrome c release,
Bcl-2 also
regulates Smac release, suggesting that both molecules may escape via the same route
Sun et al., J Biol Chem 2002
:
Importantly,
Bcl-2 and Bcl-x ( L )
inhibited the release of both cytochrome c and
Smac from mitochondria
Fulda et al., Oncogene 2002
(Breast Neoplasms...) :
In contrast, in SKW lymphoblastoid cells, TRAIL induced activation of caspase-8 directly translated into full activation of caspases, cleavage of XIAP, DFF45 or PARP and apoptosis independent of Bcl-2 overexpression, although
Bcl-2 similarly
inhibited loss of mitochondrial membrane potential and the release of cytochrome c, AIF and
Smac from mitochondria in all cell types
Sinicrope et al., Clin Cancer Res 2004
(Colonic Neoplasms) :
Bcl-2 inhibited TRAIL induced Bax translocation, cytosolic release of cytochrome c and
Smac/DIABLO , and the downstream cleavage of XIAP and DFF45
Hui et al., Diabetes 2005
:
All three agents
induce a decrease of intracellular levels of Bcl-2 and
Bcl-xL , with an increased level of
Smac , indicating that they are capable of promoting a downregulation of anti-apoptotic factors and an accumulation of pro-apoptotic mediators
Yao et al., J Neurosci 2005
(Alzheimer Disease) :
We observed that
Smac release was
potentiated by suppression of
Bcl-w and reduced by overexpression of Bcl-w
Fulda et al., Eur J Cancer 2005
:
While resveratrol enhanced TRAIL induced apoptosis through G1 cell cycle arrest and survivin depletion, resveratrol failed to sensitise cells with high expression levels of Bcl-2 or FADD-DN. Interestingly, overexpression of
Bcl-2 or FADD-DN did not interfere with resveratrol mediated cell cycle arrest or survivin depletion, but
blocked release of cytochrome c and
Smac from mitochondria into the cytosol, enhanced caspase activation and apoptosis upon combined treatment with resveratrol and TRAIL indicating that overexpression of Bcl-2 or FADD-DN decoupled the effect of resveratrol on the cell cycle and apoptosis
Korga et al., Pol Merkur Lekarski 2006
(Neoplasms) :
Special attention was paid to the defects of transduction of apoptotic signals in chemoresistant tumor cells such as alteration in expression of IAP and
Bcl-2-family and
role of
Smac/Diablo as an agent, which analyzed deeply may contribute to create new forms of anticancer therapies
Górka et al., Cell Mol Biol Incl Cyto Enzymol 2006
(Breast Neoplasms) :
Bid knock down and
Bcl-2 overexpression delayed Bax-GFP aggregation and completely
inhibited Smac/DIABLO-GFP release from mitochondria
Das et al., J Neurooncol 2008
(Brain Neoplasms...) :
The events of apoptosis included increase in expression of Bax, down
regulation of
Bcl-2 and baculoviral inhibitor-of-apoptosis protein (IAP) repeat containing ( BIRC ) proteins, mitochondrial release of cytochrome c and
Smac into the cytosol, increase in intracellular free [ Ca ( 2+ ) ], and activation of calpain, caspase-9, and caspase-3