scholarly journals Caspase-9 cleavage, do you need it?

2007 ◽  
Vol 405 (1) ◽  
Author(s):  
Davina Twiddy ◽  
Kelvin Cain
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Caspase 9 ◽  
Autocatalytic Cleavage ◽  
Downstream Effector ◽  
Apoptosis Inhibition ◽  
Biochemical Journal ◽  
Effector Caspase ◽  
Effector Caspases

Caspase-9, which is activated by association with the Apaf-1 (apoptotic protease-activating factor-1) apoptosome complex, cleaves and activates the downstream effector caspases-3 and -7, thereby executing the caspase-cascade and cell-death programme. Although caspase-9 does not need to be cleaved to be active, apoptotic cell death is always accompanied by autocatalytic cleavage and by further downstream effector caspase-dependent cleavage of caspase-9. In this issue of the Biochemical Journal, Denault and co-workers evaluate the role of caspase-3-dependent cleavage of caspase-9 and conclude that this mechanism mainly serves to enhance apoptosis by alleviating XIAP (X-linked inhibitor of apoptosis) inhibition of the apical caspase.

scholarly journals Voltage-dependent anion channels mediated apoptosis in refractory epilepsy

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 745-753
Author(s):  
Yan Zhao ◽  
Wen-Jing Jiang ◽  
Lin Ma ◽  
Yan Lin ◽  
Xing-Bang Wang
Keyword(s):  
Cell Death ◽  
Essential Role ◽  
Refractory Epilepsy ◽  
Apoptotic Cell ◽  
Anion Channel ◽  
Anion Channels ◽  
Voltage Dependent Anion Channel ◽  
Caspase 9 ◽  
Voltage Dependent

AbstractThe purpose of this study was to investigate the role of voltage-dependent anion channel (VDAC) in mitochondria-mediated apoptosis of neurons in refractory epilepsy. Western blot analyses were carried out to detect the changes in cytochrome C, caspase 9, Bax, and Bcl-2. TUNEL assays were also carried out to investigate cell apoptosis under the upregulation and downregulation of VDAC1 with or without Bax or Bcl-2. VDAC1 induced Bax, Bcl-2, and caspase 9, increasing the release of cytochrome C. VDAC1 played an essential role in the apoptotic cell death of refractory epilepsy. It is concluded that VDAC1 plays an important role in refractory epilepsy and could be a possible therapeutic target of anti-epileptic drugs. The current study provides a new understanding of the possible mechanisms of refractory epilepsy.

scholarly journals Uncouplers of Oxidative Phosphorylation Can Enhance a Fas Death Signal

1999 ◽  
Vol 19 (5) ◽  
pp. 3299-3311 ◽  
Author(s):  
Georg Linsinger ◽  
Sabine Wilhelm ◽  
Hermann Wagner ◽  
Georg Häcker
Keyword(s):  
Oxidative Phosphorylation ◽  
Mitochondrial Membrane ◽  
Apoptotic Cell ◽  
Jurkat Cells ◽  
Inner Mitochondrial Membrane ◽  
Caspase 9 ◽  
Intact Cells ◽  
Effector Caspases ◽  
Carbonyl Cyanide

ABSTRACT Recent work suggests a participation of mitochondria in apoptotic cell death. This role includes the release of apoptogenic molecules into the cytosol preceding or after a loss of mitochondrial membrane potential ΔΨm. The two uncouplers of oxidative phosphorylation carbonyl cyanide m-chlorophenylhydrazone (CCCP) and 2,4-dinitrophenol (DNP) reduce ΔΨm by direct attack of the proton gradient across the inner mitochondrial membrane. Here we show that both compounds enhance the apoptosis-inducing capacity of Fas/APO-1/CD95 signaling in Jurkat and CEM cells without causing apoptotic changes on their own account. This amplification occurred upstream or at the level of caspases and was not inhibited by Bcl-2. The effect could be blocked by the cowpox protein CrmA and is thus likely to require caspase 8 activity. Apoptosis induction by staurosporine in Jurkat cells as well as by Fas in SKW6 cells was unaffected by CCCP and DNP. The role of cytochrome c during Fas-DNP signaling was investigated. No early cytochrome c release from mitochondria was detected by Western blotting. Functional assays with cytoplasmic preparations from Fas-DNP-treated cells also indicated that there was no major contribution by cytochrome c or caspase 9 to the activation of effector caspases. Furthermore, an increase of rhodamine-123 uptake into intact cells, which has been explained by mitochondrial swelling, occurred considerably later than the caspase activation and was blocked by Z-VAD-fmk. These data show that uncouplers of oxidative phosphorylation can presensitize some but not all cells for a Fas death signal and provide information about the existence of separate pathways in the induction of apoptosis.

scholarly journals The flower pot method of REM sleep deprivation causes apoptotic cell death in the hepatocytes of rat

2018 ◽  
Author(s):  
Atul Pandey ◽  
Devesh Kumar ◽  
Gopesh Ray ◽  
Santosh Kar
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Sleep Deprivation ◽  
Rem Sleep ◽  
Protein Level ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Caspase 9

AbstractIntroductionThe rapid eye movement sleep deprivation (REMSD) of rats relates with increased inflammations, acute phase response, oxidative damage, neuronal cell loss, and neurodegenerative diseases. Whereas, its role outside brain are not well studied. This study tried to explore the causal effect of REM sleep loss on hepatocytes.MethodsWe deprived the rats of REM sleep using standard flower pot method. We focused on liver to see the REMSD affects which controls most of the metabolic processes of the body.ResultsWe report here that flower pot induced REMSD causes apoptotic cell death of hepatocytes (~10% by Annexin Assay & ~20% by TUNEL assay). This were further got alleviated up to extent after sleep recovery of 5 days (recovered approximately 8.0% by Annexin Assay & 14% by TUNEL assay). The gene expression and protein level profiling revealed the up-regulation of p53, Bax, Cytochrome c, Caspase 3, and Caspase 9. While, Bcl2 which is an anti-apoptotic protein were down-regulated in response to REMSD. Relentless recovery of 5 days affected the expression pattern of these genes/proteins.ConclusionsOur study offer great pathological and physiological significance for sleep loss, by inferring the apoptotic cell-death in the hepatocytes of rat. This further signifies the functional and preventive role of REM sleep which is unique to mammals and avians with certain exceptions, as its loss can affect the natural well-being and survival of the individuals.Highlights of the studyWe observed significant apoptosis in the hepatocytes of REMSD group of rats.Our expression analysis confirmed altered expression for genes p53, Bcl2, Bax, and Caspase-3 after REMSD.Protein level analysis supported our gene expression results for p53, Bcl2, Bax, Caspase 3 and Caspase 9 after REMSD.Sleep recovery improved the respective genes and protein expression levels towards normalcy, signifying the functional role of REM sleep.

scholarly journals Adenovirus encoding HIV-1 Vpr activates caspase 9 and induces apoptotic cell death in both p53 positive and negative human tumor cell lines

Oncogene ◽  
2002 ◽  
Vol 21 (30) ◽  
pp. 4613-4625 ◽  
Author(s):  
Karuppiah Muthumani ◽  
Donghui Zhang ◽  
Daniel S Hwang ◽  
Sagar Kudchodkar ◽  
Nathanael S Dayes ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Cell ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Human Tumor ◽  
Tumor Cell Lines ◽  
Caspase 9 ◽  
Human Tumor Cell ◽  
Human Tumor Cell Lines ◽  
Hiv 1

Proinflammatory phenotype of coronary arteries promotes endothelial apoptosis in aging

2004 ◽  
Vol 17 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Anna Csiszar ◽  
Zoltan Ungvari ◽  
Akos Koller ◽  
John G. Edwards ◽  
Gabor Kaley
Keyword(s):  
Cell Death ◽  
Coronary Arteries ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
The Elderly ◽  
Apoptotic Cell Death ◽  
Caspase 9 ◽  
No Donor ◽  
Endothelial Apoptosis ◽  
Age Related

Previously we demonstrated that aging in coronary arteries is associated with proinflammatory phenotypic changes and decreased NO bioavailability, which, we hypothesized, promotes vascular disease by enhancing endothelial apoptosis. To test this hypothesis we characterized proapoptotic alterations in the phenotype of coronary arteries of aged (26 mo old) and young (3 mo old) F344 rats. DNA fragmentation analysis and TUNEL assay showed that in aged vessels there was an approximately fivefold increase in the number of apoptotic endothelial cells. In aged coronary arteries there was an increased expression of TNFα, TNFβ, and caspase 9 (microarray, real-time PCR), as well as increased caspase 9 and caspase 3 activity, whereas expression of TNFR1, TNFα-converting enzyme (TACE), Bcl-2, Bcl-X(L), Bid, Bax, caspase 8, and caspase 3 were unchanged. In vessel culture (18 h) incubation of aged coronary arteries with a TNF blocking antibody or the NO donor S-nitroso-penicillamine (SNAP) decreased apoptotic cell death. Incubation of young arteries with exogenous TNFα increased caspase 9 activity and elicited endothelial apoptosis, which was attenuated by SNAP. Inhibition of NO synthesis in cultured young coronary arteries also induced apoptotic cell death and potentiated the apoptotic effect of TNFα. Thus we propose that age-related upregulation of TNFα and caspase 9 and decreased bioavailability of NO promote endothelial apoptosis in coronary arteries that may lead to impaired endothelial function and ischemic heart disease in the elderly.

Mixed-ligand copper(ii) Schiff base complexes: the vital role of co-ligands in DNA/protein interactions and cytotoxicity

2017 ◽  
Vol 41 (3) ◽  
pp. 1267-1283 ◽  
Author(s):  
Sellamuthu Kathiresan ◽  
Subramanian Mugesh ◽  
Jamespandi Annaraj ◽  
Maruthamuthu Murugan
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Schiff Base ◽  
Protein Interactions ◽  
Apoptotic Cell ◽  
Vital Role ◽  
Mixed Ligand ◽  
Schiff Base Complexes ◽  
Antibacterial Mechanism

Four new mixed-ligand copper(ii) complexes display an antibacterial mechanism of cell death via cell-wall rupture and cytotoxicity via apoptotic cell death.

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