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CASP5 — CDK2
Text-mined interactions from Literome
Kim et al., Oncogene 2001
(Stomach Neoplasms) :
In contrast, the suppression of
caspase-3 activity
inhibited the cleavage of target proteins, the activation of
Cdk2 , and the induction of apoptosis
Morris et al., J Neurosci 2001
:
However, either p53 deficiency or the inhibition of
CDK activity alone
inhibited Bax translocation, cytochrome c release, and
caspase-3-like activation
Hiromura et al., Oncogene 2002
:
Finally, we showed that
caspase-3 activity was significantly
reduced by inhibiting
CDK2 activity with Roscovitine
Lukovic et al., Exp Cell Res 2003
:
Employing direct cytofluorimetric analyses of intracellular caspase activity and colony forming assays, we now show that transient blockade of
caspase dependent
Cdk2 activity confers long lived sparing from death on cells otherwise triggered to die and fully replete with caspase activity
Sohn et al., Cancer Res 2006
:
p21 blocks irradiation induced apoptosis downstream of mitochondria by inhibition of
cyclin dependent kinase mediated
caspase-9 activation
Wu et al., Planta Med 2007
:
The mechanisms underlying these pharmacological effects include reduced expression of cell cycle mediators such as CDK4, cyclins D1 and A, retinoblastoma ( Rb ) and vascular endothelial growth factor receptor 1 ( VEGFR-1 ), and promotion of
caspase mediated
activation of
CDK inhibitors p21(Cip1) and p27 ( Kip )
Wang et al., J Asian Nat Prod Res 2009
:
1 in high concentrations
induced Bax,
caspase-3 , and cyclin dependent kinase (CDK) inhibitor P21 expression, whereas the expressions of cyclin
CDK2 , Bcl-2, and proliferating cell nuclear antigen ( PCNA ) were decreased by 1 treatment
Yang et al., Mol Med Report 2010
:
The expression of cyclin D1
, cyclin dependent kinase 4 (CDK4), Bcl-2, Bcl-xL and
the activation
of caspase-3 were examined by Western blotting
Guo et al., Protein & cell 2011
:
Ectopic expression of the dominant negative
Cdk2 ( Cdk2-dn ) and a specific Cdk2 inhibitor, p21 ( WAF1/CIP1 ), effectively
suppresses the loss of MMP, the release of cytochrome c, and subsequent activation of
caspase-3 in paclitaxel treated cells