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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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BCL3 — CASP14

Text-mined interactions from Literome

Ozaki et al., J Biol Chem 1999 : Apoptosis was induced in human glioma cell lines by exposure to 100 nM calphostin C, a specific inhibitor of protein kinase C. Calphostin C-induced apoptosis was associated with synchronous down-regulation of Bcl-2 and Bcl-xL as well as activation of caspase-3 but not caspase-1
Miho et al., Cell Death Differ 1999 : Bcl-xL inhibited the activation of caspase-3-like proteases
Carthy et al., Lab Invest 1999 : Bcl-2 or Bcl-xL overexpression delayed morphologic changes, depressed caspase activation, and limited substrate degradation, but did not protect against loss of viability after verteporfin photosensitization
de la Coste et al., Am J Physiol 1999 : Bcl-xL and Bcl-2 were protective without any change in the level of endogenous Bcl-xL or Bax and inhibited hepatic caspase-3-like activity
Newmeyer et al., Cell Death Differ 2000 : These observations, together with previous results obtained with Bcl-2, argue that Bcl-xL and Bcl-2 can not block the apoptosome mediated activation of caspase-9
Nakagawa et al., J Cancer Res Clin Oncol 2000 (Breast Neoplasms) : The apoptosis cascade was due to up-regulation of Bax protein, down-regulation of Bcl-XL protein, and activation of caspase-3
Herrera et al., Hepatology 2001 : However, caspase activation mediates cleavage of Bid and Bcl-xL that could originate an amplification loop on the mitochondrial events
Gollapud et al., J Clin Immunol 2001 : Induction of apoptosis was associated with increased expression of CD95L ; activation of caspase 3, however, did not affect the expression of Bcl-2 and Bcl-xL
Lamothe et al., J Interferon Cytokine Res 2002 (Leukemia, Promyelocytic, Acute) : Overall, these results indicate that TRAIL induced apoptosis involves activation of caspase-8 , caspase-7, caspase-3, and BID cleavage, and Bcl-2 and Bcl-xL prevents TRAIL induced apoptosis by abrogating caspase activation and BID cleavage
Nitta et al., Exp Cell Res 2002 : Overexpression of Bcl-xl , an anti-apoptotic Bcl-2 family protein, completely inhibited Delta psi m disruption, caspase activation, and cell death
Cao et al., J Neurosci 2002 (Ischemic Attack, Transient) : Finally, as shown by immunohistochemistry, Western blotting, and substrate-cleavage assays, PTD-HA-Bcl-xL attenuated ischemia induced caspase-3 activation in ischemic neurons
Jang et al., Biochem Biophys Res Commun 2002 : Arginine antimetabolite L-canavanine induces apoptotic cell death in human Jurkat T cells via caspase-3 activation regulated by Bcl-2 or Bcl-xL ... The L-canavanine induced caspase-3 activation, degradation of PARP, and apoptotic DNA fragmentation were suppressed by ectopic expression of Bcl-2 or Bcl-xL , both of which are known to play roles as anti-apoptotic regulators
Chen et al., Acta Pharmacol Sin 2002 (Parkinsonian Disorders) : Rg1 has protective effect against MPTP induced apoptosis and this effect may be attributed to enhancing Bcl-2 and Bcl-xl expression, reducing Bax and iNOS expression, and inhibiting activation of caspase-3
Emanuele et al., Int J Oncol 2002 (Hepatoblastoma...) : Apoptosis induced in hepatoblastoma HepG2 cells by the proteasome inhibitor MG132 is associated with hydrogen peroxide production, expression of Bcl-XS and activation of caspase-3
Bae et al., Biochem Biophys Res Commun 2003 : Curcumin induces apoptosis in U937 cells via a mechanism that appears to involve down-regulation of the anti-apoptotic Bcl-xL , and IAP proteins, release of cytochrome c, and activation of caspase 3
Petak et al., Cell Death Differ 2003 (Rhabdomyosarcoma) : Bcl-xL did not inhibit the early activation of caspase-8 ( < 4 h ) but inhibited cleavage of Bid, suggesting that Bid is cleaved downstream of the mitochondria, independent of caspase-8
Blanco-Colio et al., Kidney Int 2003 : The overexpression of Bcl-xL also prevented the activation of caspase 9 and 3
Reimertz et al., J Cell Biol 2003 : Expression of Bbc3/PUMA correlated with a Bcl-xL-sensitive release of cytochrome c and the activation of caspase-9 and -3
Carthy et al., Virology 2003 (Coxsackievirus Infections) : Enforced Bcl-2 and Bcl-xL expression markedly reduced release of cytochrome c, presentation of the mitochondrial epitope 7A6, and depressed caspase activation following infection
Cantara et al., J Vasc Res 2004 : Hydrogen peroxide induced apoptosis is mediated through the inhibition of Bcl-xl activity and caspase-3 and caspase-9 activation
Mühlethaler-Mottet et al., Oncogene 2004 (Neuroblastoma) : Drug mediated sensitization to TRAIL induced apoptosis in caspase-8 complemented neuroblastoma cells proceeds via activation of intrinsic and extrinsic pathways and caspase dependent cleavage of XIAP, Bcl-xL and RIP
Sonnemann et al., Cancer Lett 2004 (Lung Neoplasms) : Down-regulation of either PKCeta or Bcl-xL in combination with vincristine or paclitaxel resulted in a significant increase in caspase-3 activity compared to that in the control oligonucleotide treated cells
Yacoub et al., Cancer Biol Ther 2004 (Brain Neoplasms...) : Inhibition of caspase 9 after combination treatment blunted neither JNK1/2/3 activation nor the enhanced expression of BAD and BAX, but did block caspase 3 cleavage, reduced expression of BCL-XL and inhibition of ERK1/2 activity
Rashmi et al., Carcinogenesis 2004 (Colonic Neoplasms) : Curcumin induced activation of caspase 8 was blocked by Ku70 but not by Bcl-XL
Klein et al., Biochem Biophys Res Commun 2004 : Spontaneous caspase activation in human islets and cytotoxicity caused by IL-1beta were significantly reduced in the presence of TAT-Bcl-XL and TAT-BH4
Shimizu et al., Clin Cancer Res 2004 (Carcinoma, Hepatocellular...) : Combined treatment with low concentrations of these two agents also acted synergistically to induce apoptosis in HepG2 cells through induction of Bax and Apaf-1, reduction of Bcl-2 and Bcl-xL , and activation of caspase-3 , -8, and -9
Huang et al., Eur J Pharmacol 2004 (Prostatic Neoplasms) : Taken together, it is suggested that caseamembrin C-induced apoptosis is predominantly through the activation of intrinsic apoptosis pathways by causing the down-regulation of Bcl-2 and Bcl-xL expression, up-regulation of Mcl-1S protein and activation of caspase-9 and caspase-3
Kawano et al., Anticancer Res 2004 (MAP Kinase Signaling System) : The combination treatment activated caspase-3 and cleaved PARP, but it did not induce any notable change in the expression of Bcl-XL , Bcl-2 and Bax compared with each single treatment
Kim et al., Toxicological sciences : an official journal of the Society of Toxicology 2005 : The selective COX-2 inhibitor, NS-398, potentiated the 2,2',4,6,6'-PeCB induced mitochondrial apoptotic pathway involved in Bcl-xL attenuation, cytochrome c release and the subsequent activation of caspase-3
Kim et al., Oncol Rep 2004 (Adenocarcinoma) : Methyl jasmonate induces apoptosis through induction of Bax/Bcl-XS and activation of caspase-3 via ROS production in A549 cells ... Herein we show that methyl jasmonate induces apoptosis through induction of Bax/Bcl-XS and activation of caspase-3 via reactive oxygen species production in A549 human lung adenocarcinoma cells
Lorz et al., Kidney Int 2005 : The decrease in Bcl-xL was prevented by lactacystin, but not by caspase inhibitors
Chang et al., Life Sci 2005 (Carcinoma, Hepatocellular...) : Increase in Bax/ Bcl-XL ratio and activation of caspase-3 supported the apoptotic finding on gel electrophoresis
Rohrbach et al., J Mol Cell Cardiol 2005 : Attenuating erbB signals in cultured neonatal rat cardiomyocytes by the erbB2 antagonist tyrphostin AG825, by the erbB1/4 antagonist AG1478 or by antisense induced lowering of erbB2 receptors resulted in an augmented Bcl-xS/Bcl-xL ratio, mitochondrial release of cytochrome c, activation of caspase 9 and caspase 3, and nucleosome sized DNA fragmentation
Zhu et al., Oncogene 2005 (Colonic Neoplasms...) : To characterize the mechanisms of apoptosis induction by proteasome inhibitors, we examined levels of Bcl-2 protein family members ( Bik/NBK, Bax, Bak, Bcl-2, and Bcl-XL ), release of cytochrome c, and activation of caspase-9 and -3 in human colon cancer cell lines DLD1, LOVO, SW620, and HCT116 ; human lung cancer cell line H1299 ; and human ovarian cancer cell line SKOV3 after they were treated with bortezomib
Wang et al., J Biol Chem 2006 : The decrease in Bcl-xL was not blocked by a caspase 3 inhibitor but blocked in both DT40-hTRX2 and DT40-hTRX2CS
Klumpp et al., Infect Immun 2006 (Escherichia coli Infections...) : Consistent with this possibility, overexpression of Bcl ( XL ) inhibited NU14 activation of caspase 3
Yacoub et al., Mol Pharmacol 2007 (Prostatic Neoplasms) : The promotion of hCG lethality by lovastatin was abolished by overexpression of BCL- ( XL ), and was dependent upon activation of caspase-9
Liu et al., Ann Hematol 2007 (Leukemia) : Taken together, our results demonstrate for the first time that downregulation of cyclooxygenase-2 expression, disruption of mitochondrial membrane potential, activation of caspase-3 , downregulation of Bcl-2, Bcl-Xl , and Mcl-1, and upregulation of Bax are involved in PPAR-gamma agonists induced apoptosis in these two human monocyte leukemia cells
Bruey et al., Cell 2007 (Inflammation) : Bcl-2 and Bcl-XL regulate proinflammatory caspase-1 activation by interaction with NALP1
Yang et al., J Vasc Res 2007 (Carotid Artery Diseases) : Resistance to fas induced apoptosis in cells from human atherosclerotic lesions : elevated Bcl-XL inhibits apoptosis and caspase activation
Chen et al., J Biol Chem 2007 : We observed that caspase-9 dimerization resulted in the loss of mitochondrial membrane potential and the cleavage of anti-apoptotic Bcl-2, Bcl-xL , and Mcl-1
Shyu et al., J Clin Invest 2008 (Cerebral Infarction...) : SN also induced expression of the antiapoptotic proteins Bcl-2 and Bcl-xL through the Jak2/Stat3 pathway and inhibited apoptosis by blocking caspase-3 activation
Cai et al., Sarcoma 2000 : Paclitaxel induced cell cycle arrest with an accumulation of cells in sub-G1.This was accompanied in vitro by various events typical of apoptosis : phosphorylation of two anti-apoptotic proteins Bcl-2 and Bcl- ( xL ), release of cytochrome c into the cytoplasm, cleavage and activation of caspase-3
Zhang et al., International journal of clinical and experimental pathology 2008 : Furthermore, ectopic expression of exogenous Bcl-xL via adenoviral vector prevented H ( 2 ) O ( 2 ) -triggered caspase-3 activation
Zucchini-Pascal et al., Toxicology 2009 (Necrosis) : This disruption of cell suicide was linked to Bcl-xL up-regulation, Bax down-expression, prevention of cytochrome c release, and inhibition of caspase-9 and -3 activities
Palozza et al., J Nutr Biochem 2010 : Concomitantly, it inhibited 7-KC induced apoptosis, by limiting caspase-3 activation and the modulatory effects of 7-KC on AKT, Bcl-2, Bcl-xL and Bax
Antczak et al., J Biomol Screen 2009 : Overexpression of the antiapoptotic protein Bcl-XL , alone or in combination with the inhibitor Z-VAD-FMK, attenuated caspase activation in HeLa cells exposed to doxorubicin, etoposide, or cell death siRNA
Kumar et al., J Am Soc Nephrol 2009 (Reperfusion Injury) : In rat renal IRI, a single dose of dexamethasone administered before ischemia, or at the onset of reperfusion, ameliorated biochemical and histologic acute kidney injury after 24 h. Dexamethasone upregulated Bcl-xL , downregulated ischemia induced Bax, inhibited caspase-9 and caspase-3 activation, and reduced apoptosis and necrosis of proximal tubular cells
Geng et al., Biol Pharm Bull 2010 : Abeta induced c-Jun N-terminal kinase (JNK) results in phosphorylation, subsequent down-regulation of Bcl-2 and Bcl-w expression, and caspase-3 activation
Zhang et al., Cell Biochem Funct 2010 (Diabetes Mellitus, Type 2) : The results showed that treatment with GlcN induced HIT-T15 cell death via apoptotic pathway, inhibited the expression of Bcl-2 and Bcl-xL , enhanced the expression of Bax, Bid and caspase-3 , reduced the production of ATP and decreased in insulin secretion
Das et al., Proc Natl Acad Sci U S A 2010 (Prostatic Neoplasms) : Cotreatment with sildenafil enhanced DOX induced apoptosis in PC-3 and DU145 prostate cancer cells, which was mediated by enhanced generation of reactive oxygen species, up-regulation of caspase-3 and caspase-9 activities, reduced expression of Bcl-xL , and phosphorylation of Bad
Choi et al., Chem Biol Interact 2011 (Carcinoma, Renal Cell...) : Cafestol induced apoptosis is associated with the reduction of mitochondrial membrane potential ( MMP ), activation of caspase 3, cytochrome c release, and down-regulation of anti-apoptotic proteins ( Bcl-2, Bcl-xL , Mcl-1 and cFLIP )
Bagchi et al., Cytokine 2013 : Concomitantly, an increase in Bcl-xL activity inhibited Bax and the proteolytic activity of caspase 3 as well as a decrease in PARP cleavage
Guerrero et al., J Immunol 2013 : This indicates that caspase mediated cleavage of anti-apoptotic Bcl-2 or Bcl-xL facilitates AICD in T cells, whereas upregulation of Bcl-xL promotes T cell survival and allows further T cell activation
Wang et al., PloS one 2012 (Liver Neoplasms) : Z-VAD-fmk ( caspase inhibitor ), pifithrin-a ( p53 inhibitor ), or overexpressed Bcl-xl decreased the effects of quercetin on DOX mediated apoptosis
Zhang et al., Acta Pharmacol Sin 2013 (Gallbladder Neoplasms) : In GBC-SD cells, icariin significantly inhibited both the constitutive and gemcitabine induced NF-?B activity, enhanced caspase-3 activity, induced G ( 0 ) -G ( 1 ) phase arrest, and suppressed the expression of Bcl-2, Bcl-xL and surviving proteins
Yang et al., Apoptosis 2013 (Osteosarcoma) : GP7 or etoposide induced sub-G1 peak, apoptotic DNA fragmentation, activations of caspase-3 , -8, -9, and DNA fragmentation factor, downregulation of Bcl-2 and Bcl-xL , upregulation of Bax and Bak, and cytochrome-c release from mitochondria in both mouse and human OS cells
Liu et al., Oncol Rep 2013 (Breast Neoplasms) : Also, HYL-6d treatment induced MCF-7 cell apoptosis and this was accompanied by a decreased expression of Bcl-2, increased levels of p53 and Bcl-XS and the activation of caspase-9
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
Yang et al., Int Immunopharmacol 2013 (Disease Models, Animal...) : XN significantly decreased malondialdehyde, potentiated superoxide dismutase and glutathione peroxidase, reduced Bax expression, promoted Bcl-xL and inhibited caspase 3 activity in liver tissues compared with the animals without XN intervention
Kitanaka et al., Oncogene 1997 : Caspase dependent apoptosis of COS-7 cells induced by Bax overexpression : differential effects of Bcl-2 and Bcl-xL on Bax induced caspase activation and apoptosis
Scaffidi et al., EMBO J 1998 : However, in type II but not type I cells, overexpression of Bcl-2 or Bcl-xL blocked caspase-8 and caspase-3 activation as well as apoptosis
Hu et al., Proc Natl Acad Sci U S A 1998 : Expression of Bcl-XL inhibited the association of Apaf-1 with caspase-9 in mammalian cells ... Furthermore, Bcl-XL failed to inhibit caspase-9 processing mediated by a constitutively active Apaf-1 mutant, suggesting that Bcl-XL regulates caspase-9 through Apaf-1
Nagane et al., Proc Natl Acad Sci U S A 1998 (Glioblastoma) : Ectopic overexpression of Bcl-XL in parental U87MG cells also resulted in suppression of both caspase activation and apoptosis induced by CDDP
Lindenboim et al., Neurosci Lett 1998 : Our findings also showed that TNF alpha induced activation of caspase-3 is inhibited by overexpression of Bcl-xL , suggesting that Bcl-xL acts upstream of caspase activation
Suzuki et al., FEBS Lett 1998 : Synergistic action of R-Ras and IGF-1 on Bcl-xL expression and caspase-3 inhibition in BaF3 cells : R-Ras and IGF-1 control distinct anti-apoptotic kinase pathways ... It was also found that R-Ras and IGF-1 cooperatively induced Bcl-xL expression and inhibited caspase-3 activation
El-Assaad et al., Biochem J 1998 : Moreover, Bcl-xL , but not Bcl-2, totally inhibited a caspase-8-like activity in cell lysates stimulated with TNFalpha
Ibrado et al., Leukemia 1998 : These findings indicate that Bcl-xL overexpression does not affect Taxol induced CDK1 activity leading to G2/M transition, which temporally precedes the cytosolic cyt c-mediated cleavage and activity of caspase-3 and apoptosis
MacDonald et al., J Exp Med 1999 : Overexpression of Bcl-2 and Bcl-XL suppressed caspase activation, mitochondrial cytochrome c release, Deltapsi suppression, and apoptosis and cell death induced by GraB, GraK, or perforin