Apoptosis is a controlled form of cellular demolition, catalyzed by a family of cysteine proteases called caspases. In response to diverse proapoptotic stimuli, caspase-9 is recruited and activated within an oligomeric complex called the apoptosome. The apoptosome drives autocatalytic processing of caspase-9, triggering a proteolytic caspase cascade that results in the biochemical and morphological changes characteristic of cell death. It is unclear why caspase-9 undergoes autocatalytic processing following apoptosome recruitment, because interdomain processing is dispensable for caspase-9 activity. A study has shed light on this issue by demonstrating that caspase-9 processing within the apoptosome promotes its displacement from the complex, leading to inactivation of this protease. Thus, autoprocessing of caspase-9 within the apoptosome serves as a molecular timer that limits the proteolytic activity of this complex through displacement of bound caspase-9 molecules. This timer mechanism may ...

TY - JOUR. T1 - Negative regulation of the Apaf-1 apoptosome by Hsp70. AU - Saleh, Ayman. AU - Srinivasula, Srinivasa M.. AU - Balkir, Levent. AU - Robbins, Paul D.. AU - Alnemri, Emad S.. N1 - Funding Information: ACKNOWLEDGEMENTS We thank the members of Robbins laboratory, especially M. Serrano, B. Baldwin, T. Kenniston and J. Mai, for technical support. We also thank Y. Lazebnik and S. H. Kaufmann for Apaf-1 and caspase-9 antibodies, respectively, and R. Morimoto for hsp70 cDNA. This work was supported by NIH grants AG14357 and AG13487 (to E.S.A.) and CA55227 (to P.D.R.). Correspondence and requests for materials should be addressed to E.S.A.. PY - 2000/8. Y1 - 2000/8. N2 - Release of cytochrome c from mitochondria by apoptotic signals induces ATP/dATP-dependent formation of the oligomeric Apaf-1-caspase-9 apoptosome. Here we show that the documented anti-apoptotic effect of the principal heat-shock protein, Hsp70, is mediated through its direct association with the caspase-recruitment ...

Because neither E2F1 overexpression nor derepression with the addition of TSA alone was able to induce Apaf-1 up-regulation in mature neurons (Figs. 4 c and 5 a), we hypothesized that this region of chromatin may be highly repressed in mature neurons. Indeed, expression of E2F1 in the presence of TSA induced a marked transcriptional increase in Apaf-1 (Fig. 5 c) and rendered mature P28 neurons sensitive to cytochrome c (Fig. 5 d). This sensitivity of P28 neurons was dependent on the up-regulation of Apaf-1, as neurons isolated from Apaf-1-deficient mice failed to undergo cytochrome c-induced apoptosis after TSA and E2F1 treatment (Fig. 5 e). These data support the model that neuronal maturation is accompanied by increased repression of Apaf-1 at the level of chromatin structure.. We tested this model directly with a chromatin immunoprecipitation (ChIP) assay using antibodies to acetylated histone 3 (AcH3), which is indicative of active chromatin, and histone 3 trimethylated on lysine 9 (MeH3K9), ...

Detailed annotation info for ENST00000348549; Caspase-9 precursor (EC 3.4.22.-) (CASP-9) (ICE-like apoptotic protease 6) (ICE-LAP6) (Apoptotic protease Mch-6) (Apoptotic protease activating factor 3) (APAF-3). [Source:Uniprot/SWISSPROT;Acc:P55211 ...

CASP10; MCH4; Caspase-10; CASP-10; Apoptotic protease Mch-4; FAS-associated death domain protein interleukin-1B-converting enzyme 2; FLICE2; ICE-like apoptotic protease ...

Expression of APAF1 (APAF-1, CED4) in cancer tissue. The cancer tissue page shows antibody staining of the protein in 20 different cancers.

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Release of cytochrome c from mitochondria by apoptotic signals induces ATP/dATP-dependent formation of the oligomeric Apaf-1-caspase-9 apoptosome. Here we show that the documented anti-apoptotic effect of the principal heat-shock protein, Hsp70, is mediated through its direct association with the ca …

The invention relates to an isolated nucleic acid molecule encoding a caspase-14 polypeptide or functional fragment thereof, a vector that contains the nucleic acid molecule and a host cell that contains the vector. The invention also relates to an isolated gene encoding caspase-14, as well as functional fragments thereof. The gene or nucleic acid molecule can include single or double stranded nucleic acids corresponding to coding or non-coding strands of the caspase-14 nucleotide sequence. Isolated caspase-14 polypeptides or functional fragments thereof are also provided, as are antibodies that specifically bind thereto. In addition, the invention relates to methods of identifying compounds that modulate caspase-14 activity.

A short pro-domain caspase that plays an effector Role in Apoptosis. It is activated by Initiator Caspases such as Caspase 3 and Caspase 10. Several Isoforms of this protein exist due to multiple Alternative Splicing of its Messenger RNA ...

CARD8 (caspase recruitment domain family, member 8), Authors: Frank A. Kruyt. Published in: Atlas Genet Cytogenet Oncol Haematol.

Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.

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Apoptotic signaling is altered at many loci in cancer cells. Although many tumors develop resistance to cytochrome c-induced apoptosis, we have discovered that breast cancer cells exhibit a unique hypersensitivity to cytochrome c-induced apoptosis. Interestingly, this sensitivity is not due to changes in core apoptosomal proteins ( 44) but is due to a PHAPI-mediated posttranslational event that enhances the recruitment of caspase-9 to the Apaf-1 CARD. These findings have the potential to affect breast cancer chemotherapy through the development of apoptosome activators or cytochrome c mimetics as shown, in principle, by the fact that malignant mammary epithelial cells could be more easily killed by cytosolic cytochrome c than their normal counterparts.. PHAPI-mediated increase in caspase activation in breast cancer. Whereas many inhibitory signaling pathways converge on the apoptosome, there are very few physiologic/pathologic examples of enhanced apoptosome activation. Our data suggest that ...

The effect was found to be associated with increased expression of E2F-1 in cervical cancer cells as there is no CAPE-mediated induction of E2F-1 in the precancerous cervical Z172 cells. CAPE also upregulated the E2F-1 target genes cyclin A, cyclin E, and apoptotic protease activation of factor 1 (Apaf-1) but down regulated cyclin B and myeloid leukemia cell differentiation protein (Mcl-1). These results suggested the involvement of E2F-1 in CAPE-mediated growth inhibition and cell cycle arrest. Transient transfection studies with luciferase reporters revealed that CAPE altered transcriptional activity of the apaf-1 and mcl-1 promoters. Further studies using chromatin immunoprecipitation (ChIP) assays demonstrated that in CAPE-treated cells, E2F-1 binding to the apaf-1 and cyclin B promoters was increased and decreased, respectively. Furthermore, E2F-1 silencing abolished CAPE-mediated effects on cell cycle arrest, apoptosis, and related gene expression ...

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The present study examined levels of various components of the cell death machinery and drug sensitivity of 60 human cancer cell lines to anticancer drugs. With the exception of procaspase-3, which was undetectable in MCF-7 cells, caspases-2, -3, -6, -7, -8, and -9, as well as Apaf-1, were detectable in all 60 cell lines. Although these components of the cell death machinery varied widely in abundance, strong correlations between levels of Apaf-1 or procaspase-2, -3, -6, -8, or -9 and sensitivity to any class of antineoplastic agent were not observed. These results, although negative, have several important implications.. The attempt to correlate drug sensitivity with levels of various components of the cell death machinery was prompted by previous studies indicating that drug-induced apoptosis is markedly diminished when certain key components of the core cell-death machinery, particularly Apaf-1, procaspase-9, or procaspase-3, are genetically or functionally deleted (36, 37, 38 , 58 , 88 , 99) ...

Diva (death inducer binding to vBcl-2 and Apaf-1) is a Bcl-2 family member, and has been reported to play roles in apoptosis and oocyte maturation. Diva has also been shown to interact with Nm23-H2/NDPK B, which is involved in cellular differentiation. The main aim of this study was to elucidate the function and possible mechanisms for Diva in cellular differentiation in the brain. In the present study, in PC-12 cells, Diva expression was decreased after differentiation and reciprocally, NDPK B expression was increased and it translocated into the nucleus. Endogenous Diva was also shown to interact with both ß-tubulin and NDPK B. Overexpression of Diva in PC-12 cells did not change the expression level of NDPK B, but inhibited its nuclear localization. Diva-overexpressing cells had a decreased percentage of differentiated cells and average neurite length was shortened. This was due to the formation of more Diva/NDPK B and Diva/ß-tubulin complexes, at the expense of NDPK B/ß-tubulin complexes. ...

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Chris Cory is currently on a nationwide tour with DIVA DOG, partnering with animal rescue groups and pit bull advocacy organizations. So far, we have brought DIVA DOGs message to LA, Philadelphia, Portland (OR), Kansas City, Fredericksburg (VA) and now Toronto. We are starting to go international! Hoping to bring DIVA DOG to the UK by Labor Day.. The next stops on the DIVA DOG tour are Montclair (NJ), NYC and Birmingham(AL). Woo-hoo! All upcoming events info is in our Monthly Newsletter/E-Zine. Keep on the lookout for some new and exciting DIVA DOG events in July and August to commemorate Coral the Diva Dogs birthday July 23. We will be working with a wonderful rescue called Mariahs Promise in Colorado and bringing DIVA DOG right to the Denver area, where BSL (breed-specific legislation) is really destroying homes and families, as pit bulls are ripped from their families based soley upon their breed. To learn more about the seriousness of this issue and how BSL is something that MUST be ...

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CARD9 antibody [N1N3] (caspase recruitment domain family, member 9) for IHC-P, WB. Anti-CARD9 pAb (GTX110789) is tested in Human, Mouse samples. 100% Ab-Assurance.

Curators comment: (updated: 22 Mar 2007 23:30:25 GMT). The simulation image shown corresponds to active caspase-3 temporal evolution for Apaf-1 concentration of 20nM as depicted in Fig-2A of the paper. Result obtained from MathSBML.. ...

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The apoptosome is the cellular structure that facilitates programmed cell death. A new 3D map of it lays groundwork for future drug development.

14-3-3 tau mediates E2F1 stabilization. 14-3-3 tau interacts with ATM-phosphorylated E2F1 during DNA damage and inhibits E2F1 ubiquitination. 14-3-3 tau is also required for expression and induction of E2F1 apoptotic targets, such as p73, Apaf-1, and caspases, during DNA damage ...

Expression of CASP9 (APAF-3, ICE-LAP6, MCH6, PPP1R56) in vagina tissue. Antibody staining with HPA001473, HPA046488 and CAB004348 in immunohistochemistry.

Apoptosis or programmed cell death is a process with typical morphological characteristics including plasma membrane blebbing, cell shrinkage, chromatin condensation and fragmentation. A family of cystein-dependent aspartate-directed proteases, called caspases, is responsible for the proteolytic cleavage of cellular proteins leading to the characteristic apoptotic features, e.g. cleavage of caspase-activated DNase resulting in internucleosomal DNA fragmentation. Currently, two pathways for activating caspases have been studied in detail. One starts with ligation of a death ligand to its transmembrane death receptor, followed by recruitment and activation of caspases in the death-inducing signalling complex. The second pathway involves the participation of mitochondria, which release caspase-activating proteins into the cytosol, thereby forming the apoptosome where caspases will bind and become activated. In addition, two other apoptotic pathways are emerging: endoplasmic reticulum stress-induced ...

Proteasome inhibitors including bortezomib have attracted considerable attention as potential anticancer agents, but the mechanism(s) by which proteasome inhibitors induce apoptosis is poorly understood. In the present study, we provided evidence using the human Jurkat T-cell leukemic cell line with or without stable silencing of the key adaptor protein, Apaf-1, that bortezomib-induced apoptosis but not Fas (death receptor)-mediated apoptosis is dependent on Apaf-1 expression. Furthermore, we noted that expression of Apaf-1 was variable in a panel of pediatric ALL patient samples, and Apaf-1 expression was absent altogether in one patient. The primary cells presented with a high degree of spontaneous apoptosis upon ex vivo culture; however, the Apaf-1-deficient sample presented the lowest sensitivity toward bortezomib-induced apoptosis, thus providing correlative evidence for a role of Apaf-1 in bortezomib-induced cell killing (defects in other apoptosis signaling pathways may also come into ...

As previously reported, recombinant xEIAP/XLX is rapidly degraded by at least two distinct, consecutively acting proteolytic systems [11, 14]. Within 2 h incubation, xEIAP/XLX is significantly degraded in both CSF-arrested and interphase egg extracts in a C-terminal RING finger-dependent manner. Subsequently, spontaneous cytochrome c-induced caspase activation begins after 4 h incubation in interphase egg extracts (apoptotic egg extracts), and the remaining xEIAP/XLX is cleaved by the activated caspases at yet unidentified site(s). This caspase activation is delayed or suppressed in CSF-arrested egg extracts by a p42MAPK-dependent pathway [7-11]. We found that the electrophoretic mobilities of recombinant 6XHis-tagged (6XHis-FL) and MBP-tagged (MBP-FL) xEIAP/XLX slightly decreased during incubation in CSF-arrested but not interphase egg extracts (Fig. 1B), whereas those of other BIR family proteins (xSurvivin1/xBIR1, xSurvivin2/SIX, and xXIAP) did not (data not shown). However, the rapid ...

Complete information for CARD10 gene (Protein Coding), Caspase Recruitment Domain Family Member 10, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium

Induction of apoptosis and NF-kB activation by Apaf-1/Nod1 family members and DD proteins (Inohara et al., 2000). The more recent study suggested that IKKgamma binds to the site in C-terminal regulatory region of IKKbeta which is located after the HLH motif. Images ...

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Här presenteras refereegranskade artiklar i tidskrifter författade av institutionens anställda, som har publicerats under innevarande och föregående kalenderår. Uppgifterna är hämtade från databasen DIVA.. ...