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Gene Information

Gene symbol: CASP9

Gene name: caspase 9, apoptosis-related cysteine peptidase

HGNC ID: 1511

Synonyms: MCH6, ICE-LAP6, APAF-3, PPP1R56

Related Genes

# Gene Symbol Number of hits
1 AIFM1 1 hits
2 AKT1 1 hits
3 APAF1 1 hits
4 BAK1 1 hits
5 BAX 1 hits
6 BCL2 1 hits
7 BCL2L1 1 hits
8 BID 1 hits
9 BIRC2 1 hits
10 CASP3 1 hits
11 CASP7 1 hits
12 CASP8 1 hits
13 CDK4 1 hits
14 CYCS 1 hits
15 DFFA 1 hits
16 DFFB 1 hits
17 GAP43 1 hits
18 MAPK3 1 hits
19 PARP1 1 hits
20 PCNA 1 hits
21 PIK3CA 1 hits
22 RHOD 1 hits
23 ROCK1 1 hits
24 TNF 1 hits
25 XIAP 1 hits

Related Sentences

# PMID Sentence
1 12140745 Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8.
2 12140745 In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression.
3 12140745 Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3.
4 12140745 Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8.
5 12140745 In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression.
6 12140745 Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3.
7 12840065 Here we show that codelivery of DNA encoding inhibitors of apoptosis (BCL-xL, BCL-2, XIAP, dominant negative caspase-9, or dominant negative caspase-8) with DNA encoding model antigens prolongs the survival of transduced DCs.
8 12874344 Moreover, activation of caspase 9 and the executioner caspase 3 was also observed in the LVS-infected J774A.1 macrophages.
9 12874344 The activated caspase 3 degraded poly(ADP-ribose) polymerase (PARP).
10 12874344 The internucleosomal fragmentation and PARP degradation resulting from activation of this apoptotic pathway was prevented by the caspase 3 inhibitor Z-DEVD-fmk.
11 12874344 No involvement of caspase 1, caspase 8, Bcl-2, or Bid was observed.
12 14654940 It induced cleavage of eukaryotic translation initiation factor 4G, leading to cell death through a mechanism involving activation of caspase-9, caspase-3 and poly(ADP-ribose)polymerase.
13 15869795 Cytochrome c was shown to leak from the mitochondria, followed by caspase 9 cleavage within 8 h of treatment.
14 15869795 In addition, poly(ADP-ribose) polymerase (PARP) was cleaved to form a 85 kDa fragment following maximal caspase 3 activation at 24 h.
15 17570527 HlyA oligomer-treated murine B-1a cells up-regulated TLR2 and involved the signaling molecules MyD88, TRAF6 and NF-kappaB.
16 17570527 Apoptosis was detected in majority of the monomer-treated cells that involved caspase-9 and caspase-3.
17 17881440 SH3 binding motif 1 in influenza A virus NS1 protein is essential for PI3K/Akt signaling pathway activation.
18 17881440 Recent studies have demonstrated that influenza A virus infection activates the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway by binding of influenza NS1 protein to the p85 regulatory subunit of PI3K.
19 17881440 Our previous study proposed that two polyproline motifs in NS1 (amino acids 164 to 167 [PXXP], SH3 binding motif 1, and amino acids 213 to 216 [PPXXP], SH3 binding motif 2) may mediate binding to the p85 subunit of PI3K.
20 17881440 Here we performed individual mutational analyses on these two motifs and demonstrated that SH3 binding motif 1 contributes to the interactions of NS1 with p85beta, whereas SH3 binding motif 2 is not required for this process.
21 17881440 Mutant viruses carrying NS1 with mutations in SH3 binding motif 1 failed to interact with p85beta and induce the subsequent activation of PI3K/Akt pathway.
22 17881440 Our data suggest that SH3 binding motif 1 in NS1 protein is required for NS1-p85beta interaction and PI3K/Akt activation.
23 17881440 Activation of PI3K/Akt pathway is beneficial for virus replication by inhibiting virus induced apoptosis through phosphorylation of caspase-9.
24 17982689 Lysosomal hydrolase cathepsin B (CB) is involved in the apoptotic process and has a key role in breast cancer cell programmed death through the activation of a pro-apoptotic protein BID.
25 17982689 Truncated BID participates in the mitochondrial apoptotic pathway that involves the activation of pro-caspase 9.
26 17982689 Expression of CB, BID and pro-caspase 9 was determined by Western blotting.
27 17982689 The apoptosis of T24 and MB49 cell lines was mediated by activation of pro-caspase 9 and BID, both proteins are involved in mitochondrial apoptosis.
28 17982689 Apoptosis and activation of pro-caspase 9 and BID were inhibited by CA-074Me (CA), a cell permeable CB inhibitor.
29 17982689 Lysosomal hydrolase cathepsin B (CB) is involved in the apoptotic process and has a key role in breast cancer cell programmed death through the activation of a pro-apoptotic protein BID.
30 17982689 Truncated BID participates in the mitochondrial apoptotic pathway that involves the activation of pro-caspase 9.
31 17982689 Expression of CB, BID and pro-caspase 9 was determined by Western blotting.
32 17982689 The apoptosis of T24 and MB49 cell lines was mediated by activation of pro-caspase 9 and BID, both proteins are involved in mitochondrial apoptosis.
33 17982689 Apoptosis and activation of pro-caspase 9 and BID were inhibited by CA-074Me (CA), a cell permeable CB inhibitor.
34 17982689 Lysosomal hydrolase cathepsin B (CB) is involved in the apoptotic process and has a key role in breast cancer cell programmed death through the activation of a pro-apoptotic protein BID.
35 17982689 Truncated BID participates in the mitochondrial apoptotic pathway that involves the activation of pro-caspase 9.
36 17982689 Expression of CB, BID and pro-caspase 9 was determined by Western blotting.
37 17982689 The apoptosis of T24 and MB49 cell lines was mediated by activation of pro-caspase 9 and BID, both proteins are involved in mitochondrial apoptosis.
38 17982689 Apoptosis and activation of pro-caspase 9 and BID were inhibited by CA-074Me (CA), a cell permeable CB inhibitor.
39 17982689 Lysosomal hydrolase cathepsin B (CB) is involved in the apoptotic process and has a key role in breast cancer cell programmed death through the activation of a pro-apoptotic protein BID.
40 17982689 Truncated BID participates in the mitochondrial apoptotic pathway that involves the activation of pro-caspase 9.
41 17982689 Expression of CB, BID and pro-caspase 9 was determined by Western blotting.
42 17982689 The apoptosis of T24 and MB49 cell lines was mediated by activation of pro-caspase 9 and BID, both proteins are involved in mitochondrial apoptosis.
43 17982689 Apoptosis and activation of pro-caspase 9 and BID were inhibited by CA-074Me (CA), a cell permeable CB inhibitor.
44 21288491 Since the activity of large yellow croaker caspase-9 (Lyccasp9) in the spleen and kidney also increased when the fish was stimulated with the poly(I:C) or bacterial vaccine [1], we therefore proposed that the intrinsic apoptotic pathway, which is initiated by caspase-9 and executed by caspase-3, was activated during the immune response induced by poly(I:C) or bacterial vaccine in large yellow croaker.
45 22249285 We report that hepatitis B vaccine exposure resulted in significant upregulation of the key genes encoding caspase 7, caspase 9, Inhibitor caspase-activated DNase (ICAD), Rho-associated coiled-coil containing protein kinase 1 (ROCK-1), and Apoptotic protease activating factor 1 (Apaf-1).
46 22249285 Upregulation of cleaved caspase 3,7 were detected by western blot in addition to Apaf-1 and caspase 9 expressions argues that cell death takes place via the intrinsic apoptotic pathway in which release of cytochrome c from the mitochondria triggers the assembly of a caspase activation complex.
47 22249285 We report that hepatitis B vaccine exposure resulted in significant upregulation of the key genes encoding caspase 7, caspase 9, Inhibitor caspase-activated DNase (ICAD), Rho-associated coiled-coil containing protein kinase 1 (ROCK-1), and Apoptotic protease activating factor 1 (Apaf-1).
48 22249285 Upregulation of cleaved caspase 3,7 were detected by western blot in addition to Apaf-1 and caspase 9 expressions argues that cell death takes place via the intrinsic apoptotic pathway in which release of cytochrome c from the mitochondria triggers the assembly of a caspase activation complex.
49 23119046 Vaccinia virus (VACV) encodes an anti-apoptotic Bcl-2-like protein F1 that acts as an inhibitor of caspase-9 and of the Bak/Bax checkpoint but the role of this gene in immune responses is not known.
50 23294316 Although anthocyanins induced apoptosis in some leukaemia cell lines, the level of caspase-3, caspase-8 and caspase-9 was significantly lower compared with imatinib and 6-MP.
51 23529623 Importance of PdpC, IglC, IglI, and IglG for modulation of a host cell death pathway induced by Francisella tularensis.
52 23529623 To better understand the prerequisites of this cell death, macrophages were infected with the F. tularensis live vaccine strain (LVS), and the effects were compared to those resulting from infections with deletion mutants lacking expression of either of the pdpC, iglC, iglG, or iglI genes, which encode components of the Francisella pathogenicity island (FPI), a type VI secretion system.
53 23529623 Within 12 h, a majority of the J774 cells infected with the LVS strain showed production of mitochondrial superoxide and, after 24 h, marked signs of mitochondrial damage, caspase-9 and caspase-3 activation, phosphatidylserine expression, nucleosome formation, and membrane leakage.
54 24126524 In vitro infection of bovine monocytes with Mycoplasma bovis delays apoptosis and suppresses production of gamma interferon and tumor necrosis factor alpha but not interleukin-10.
55 24126524 Here, we show that infection of bovine blood monocytes with M. bovis delays spontaneous or tumor necrosis factor alpha (TNF-α)/staurosporine-driven apoptosis, activates the NF-κB p65 subunit, and inhibits caspase-9 activity.
56 25032866 We found that apoptosis induced by M. tuberculosis is abrogated in the absence of Bak and Bax, caspase 9 or the executioner caspases 3 and 7.
57 25032866 Notably, we show that MEF deficient in the BH3-only BCL-2-interacting mediator of cell death (Bim) protein were also resistant to this process.
58 25550785 Overexpression of GRIM-19, a mitochondrial respiratory chain complex I protein, suppresses hepatocellular carcinoma growth.
59 25550785 AKT1, pAKT1, cyclinD1, CDK4, PCNA, Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3, and cytochrome C were detected by Western blot and immunofluorescence.
60 25550785 We also found that AKT1 expression and phosphorylation were regulated by the expression of GRIM-19.
61 25550785 Collectively, our study demonstrated that GRIM-19 overexpression suppressed HCC growth and downregulated AKT1 expression, suggesting that GRIM-19 might play a crucial role in hepatocarcinogenesis through negatively regulating the PI3K/AKT signaling pathway.
62 26212005 As a result, we demonstrated that the internalization of infective virus triggered the phosphorylation of ERK1/2, which was involved in the activation of caspase-9, the intrinsic pathway of apoptosis and the delivery of viral peptides on MHC class I molecules.
63 26212005 As described, infectious virus in DCs was also associated to autophagy LC3 protein and was associated to lysosomal protein Lamp-2; contrary to observe for the iFMDV.