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BCR — CASP3
Text-mined interactions from Literome
Nitta et al., Exp Cell Res 2001
:
Furthermore, addition of spermine could repress the BCR mediated apoptosis by attenuating the mitochondrial membrane potential ( Deltapsim ) loss and
activation of
caspase-7 induced by
BCR signaling
Yu et al., Cancer Res 2002
(MAP Kinase Signaling System) :
Synergistic potentiation of STI571 mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including
caspase dependent down-regulation of
Bcr-Abl and Bcl-2 ; caspase independent down-regulation of Bcl-x ( L ) and Mcl-1 ; activation of JNK, p38 MAPK, and p34 ( cdc2 ) ; and diminished phosphorylation of Stat5 and CREB
Luciano et al., FASEB J 2003
(Burkitt Lymphoma) :
We report here that
BCR triggering
leads to
caspase activation followed by Lyn cleavage and induction of apoptosis
Kim et al., Br J Haematol 2004
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
Imatinib/apicidin co-treatment for 48 h produced a prominent decrease in
Bcr-Abl protein levels in a
caspase dependent manner ... In summary, these data indicate that apicidin potentiates the imatinib induced apoptosis of Bcr-Abl positive leukaemia cells through the enhanced activation of the mitochondria dependent caspase cascades, accompanied by
caspase dependent downregulation of
Bcr-Abl and XIAP
Deming et al., Mol Cell Biol 2004
:
We report here that
Bcr-Abl also
inhibits caspase activation after the release of cytochrome c. Bcr-Abl inhibited caspase activation by cytochrome c added to cell-free lysates and prevented apoptosis when cytochrome c was microinjected into intact cells ... We report here that Bcr-Abl also inhibits caspase activation after the release of cytochrome c.
Bcr-Abl inhibited
caspase activation by cytochrome c added to cell-free lysates and prevented apoptosis when cytochrome c was microinjected into intact cells
Wang et al., Cancer Res 2005
(Leukemia, Megakaryoblastic, Acute) :
Survivin disruption in Bcr-abl transduced Mo7e cells, or in K562 cells that endogenously express Bcr-abl, by transfection with dominant negative or antisense survivin constructs promoted apoptosis induced by the Bcr-abl tyrosine kinase inhibitor STI571, which was accompanied by
caspase dependent cleavage of
Bcr-abl , mitochondrial membrane potential disruption, and enhanced mitochondrial cytochrome c release
Zhang et al., Leukemia 2008
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
We further showed that the ROS induced degradation of
BCR-ABL was
mediated partially by
caspase-3 and the proteasome pathway
Kurokawa et al., Proc Natl Acad Sci U S A 2013
(Leukemia) :
Engineering a
BCR-ABL activated
caspase for the selective elimination of leukemic cells
Lens et al., J Immunol 1998
:
Indeed, ligation of both Fas and
BCR resulted in cleavage of the IL-1beta converting enzyme/Ced-3-like protease
caspase 3 and its substrates Ac-Asp-Glu-Val-Asp-aldehyde and poly ( ADP-ribose ) polymerase