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CASP16 — CDKN1A

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Kim et al., Int J Cancer 2000 : Taken together, we suggest that UA-induced cell-cycle arrest may be mediated by inhibition of DNA replication and the increase of p21 ( WAF1 ) expression, which induces the release of cytochrome c and the activation of caspase-3 , leading to apoptosis of HepG2 cells
Naujokat et al., Eur J Haematol 2000 (Acute Disease...) : Proteasome inhibitors induced caspase dependent apoptosis and accumulation of p21WAF1/Cip1 in human immature leukemic cells
Xiang et al., Oncogene 2002 (Carcinoma...) : However, cells co-treated with CPT-11 and Apo2L/TRAIL, or pretreated with CPT-11 for up to 24 h followed by 2 h Apo2L/TRAIL, resulted in a caspase dependent degradation of p21 , reversal of G ( 2 ) -M phase arrest with a concomitant increase in apoptosis
De Schepper et al., J Pharmacol Exp Ther 2003 : Taken together, our results show that induction of apoptosis by chlamydocin involves caspase dependent cleavage of p21 ( cip1/waf1 ), which is strikingly associated with proteasome mediated degradation of survivin
Ham et al., J Biol Chem 2003 : The later phase of JNK1 activation, which is temporally coincided with caspase dependent cleavage of JNK1 associated p21 ( WAF1/CIP1 ), is efficiently prevented by expressing p21D112N, an uncleavable mutant of p21 ( WAF1/CIP1 ) and this perturbation of JNK1 activation results in prevention of apoptosis
Song et al., J Immunol 2004 (MAP Kinase Signaling System) : Furthermore, in caspase-8-deficient lymphocytes, the antiproliferative effect of CO was markedly attenuated, further supporting the involvement of caspase-8 in the antiproliferative effects of CO. CO also increased the protein level of p21 ( Cip1 ), and CO-mediated inhibition of caspase activity is partially regulated by p21 ( Cip1 )
Rosato et al., Mol Cancer Ther 2003 (Leukemia) : TRAIL/HDAC inhibitor induced apoptosis triggered caspase dependent cleavage of p21 ( WAF1/CIP1 ) ; moreover, enforced expression of a nuclear localization signal deletant form of p21 ( WAF1/CIP1 ) significantly diminished lethality
Rosato et al., Mol Pharmacol 2004 : Enforced expression of p21 ( WAF1/CIP1 ) ( i.e., in Jurkat cells inducibly expressing p21 ( WAF1/CIP1 ) under the control of a doxycycline-responsive promoter ) partially but significantly reduced cytochrome c and apoptosis inducing factor release, loss of mitochondrial membrane potential, caspase-3 and -8 activation, Bid cleavage, poly ( ADP-ribose ) polymerase ( PARP ) degradation, and apoptosis in response to SB/FP
Pei et al., Clin Cancer Res 2004 (Multiple Myeloma) : These events were associated with nuclear factor kappaB inactivation, c-Jun NH ( 2 ) -terminal kinase activation, p53 induction, and caspase dependent cleavage of p21 ( CIP1 ), p27 ( KIP1 ), and Bcl-2, as well as Mcl-1, X-linked inhibitor of apoptosis, and cyclin D1 down-regulation
Li et al., J Biol Chem 2005 : Both p21 ( waf1/cip1 ) antisense and small interfering RNA could restore apoptotic associated caspase 3 activity, PARP activation, and sensitivity to mitomycin induced apoptosis
Kosakowska-Cholody et al., Mol Cancer Ther 2005 (Colonic Neoplasms) : The recruitment of the p53 dependent apoptosis pathway was suggested by the up-regulation of p53, p21 , Bax, DR-4, DR-5, and p53 phosphorylated on Ser15 ; down-regulation of Bcl-2 ; and activation of caspase-8 , -9, -7, and -3 in cells treated with 100 nmol/L WMC-79
Rosato et al., Mol Cancer Ther 2005 (Leukemia) : LAQ824/roscovitine treated cells displayed caspase dependent down-regulation of p21 ( CIP1 ) and Mcl-1 and a pronounced caspase independent reduction in X-linked inhibitor of apoptosis (XIAP) expression
Zhang et al., J Invest Dermatol 2005 (Lymphoma, T-Cell, Cutaneous) : SAHA treatment caused an accumulation of acetylated histones ( H2B, H3, and H4 ), an increase of p21 ( WAF1 ) and bax proteins, a decrease of Stat6 and phospho-Stat6 proteins, and activation of caspase-3 in CTCL cells
Wendt et al., Oncogene 2006 (Breast Neoplasms...) : Inhibition of DNA-damage induced stress kinases and p21CIP/WAF-1 expression by caffeine abrogated G2 arrest and induced apoptosis of the irradiated cells in a caspase-3 dependent manner
Oh et al., Biochem Biophys Res Commun 2006 : Here we show that during TNFalpha induced apoptosis, PKCdelta is activated in a caspase-3 dependent manner and phosphorylates p21 ( WAF1/CIP1 ), a specific cyclin dependent kinase inhibitor, on ( 146 ) Ser
Nasu et al., Mol Hum Reprod 2005 (Endometriosis) : The down-regulation of the cyclin A, Bcl-2, and Bcl-X ( L ) expression with the simultaneous up-regulation of the p21 and Bax expression, and caspase-9 activation was observed in ECSC after bufalin treatment
Lin et al., J Urol 2006 (Urinary Bladder Neoplasms) : AE induced p53 expression and was accompanied by the induction of p21 and caspase-3 activation , which was associated with apoptosis
Tyagi et al., Carcinogenesis 2006 (Urinary Bladder Neoplasms) : Silibinin activates p53-caspase 2 pathway and causes caspase mediated cleavage of Cip1/p21 in apoptosis induction in bladder transitional-cell papilloma RT4 cells : evidence for a regulatory loop between p53 and caspase 2 ... Together, these results suggested the novel mechanisms for apoptosis induction by silibinin involving p53-caspase 2 activation and caspase mediated cleavage of Cip1/p21
Garcia et al., Cell cycle (Georgetown, Tex.) 2006 (Breast Neoplasms) : Cellular arrest in G ( 1 ) phase was accompanied by an increase in p21 ( CIP1 ) protein, down regulation of the BCL-2 protein, induction of caspase-8 , and ARHI/NOEY2 an imprinted tumor suppressor gene
Secchiero et al., Curr Drug Metab 2007 (Leukemia, Myeloid, Acute) : Moreover, while nutlin-3 up-regulated the expression of cyclin dependent kinase inhibitor p21, a p53-target gene mediating cell cycle block and showing anti-apoptotic activity, the simultaneous addition of TRAIL plus nutlin-3 induced the caspase dependent cleavage of p21
Krämer et al., Oncogene 2008 (Melanoma) : This correlates with the HU-induced degradation of the cyclin dependent kinase inhibitors ( CDKI ) p21 and p27, mediated by the proteasome or caspase-3
Baptiste-Okoh et al., Cell cycle (Georgetown, Tex.) 2008 : Further, expression of p21 ( in p53-null cells inducibly expressing p21 ) is sufficient to mediate repression of caspase 2 ... As this p53/p21 dependent repression of caspase 2 can occur in the absence of DNA damage, caspase 2 repression does not simply seem to be a consequence of the apoptotic process
Nakamura et al., Invest New Drugs 2010 (Leukemia...) : TMPP treatment effected a reduction in both cell cycle progression signals ( FoxM1, KIS, Cdc25B, Cyclin D1, Cyclin A, and Aurora-B ) and tumor cell survival ( p27 ( Kip1 ) and p21 ( Cip1 ) ), as well as induced the activation of caspase-3 and -9
Chin et al., Virus Res 2010 : This was accompanied by increased levels of p21 ( cip1 ), p-cdc2, cyclins D, A and B. Cell viability was reduced and cleaved caspase 3 levels were increased in HBV- and rtM204I infected cells
Kang et al., Oncol Rep 2010 : These results indicate that KBH-A42 induces cell cycle arrest and apoptosis via the up-regulation of p21WAF1 and caspase activation , respectively, regardless of the presence of P-gp in the leukemia cells
Bhattacharya et al., Invest Ophthalmol Vis Sci 2011 : Knockdown of p53 decreased the basal expression of p21Cip1 and Bcl-2, inhibited the Nutlin-3 induced upregulation of Siva-1 and PUMA expression, and consequently inhibited caspase-3 activation
Sohn et al., Cell Death Differ 2011 : In several cell types we show that knockdown of caspase-2 specifically impaired DNA damage induced p21 expression, whereas overexpression of a caspase-2 mutant increased p21 levels ... As, however, silencing of caspase-2 impaired exogenous expression of p21 constructs containing 3'-UTR sequences, our results strongly indicate that caspase-2 regulates p21 expression at the translational level
Chan et al., International journal of molecular sciences 2011 : In the current study, pretreatment with nitric oxide ( NO ) scavengers inhibited PDT induced mitochondrial membrane potential ( MMP ) changes, activation of caspase-9 , caspase-3, p21 activated protein kinase 2 (PAK2) and c-Jun N-terminal kinase (JNK), and gene expression of p53 and p21 involved in apoptotic signaling
Gogada et al., Cell cycle (Georgetown, Tex.) 2011 : Curcumin induces Apaf-1 dependent, p21 mediated caspase activation and apoptosis ... The release of cytochrome c was unaltered in p53-deficient cells, whereas absence of p21 blocked cytochrome c release, caspase activation, and apoptosis
Srivastava et al., Carcinogenesis 2012 : p21 deficiency caused an increase in caspase activities at lower doses of neem, whereas p53 deficiency did not modulate neem induced caspase activation
Yu et al., Biomaterials 2013 (Carcinoma, Non-Small-Cell Lung) : MDM2 knockdown in p53 mutant NSCLC H2009 cells induced significant cell cycle arrest, apoptosis and growth inhibition through upregulation of p21 and activation of caspase-3
Wang et al., PloS one 2013 (Lymphoma, B-Cell) : Meanwhile, hPEBP4 knockdown potentiated the chemosensitization of the rituximab in B-cell lymphoma cells by regulating the expression of Bcl-xl, Cycline E, p21 ( waf/cip1 ) and p53 and the activation of caspase-3 and caspase-9
Suzuki et al., Oncogene 1998 (Carcinoma, Hepatocellular) : Here we report that caspase 3 inactivation for the resistance to Fas mediated apoptosis is induced by a procaspase 3/p21 complex formation and direct inhibition of activated caspase 3 by ILP