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Study presents a structure of the Dark apoptosome at 4.4 A degrees resolution. A nearly complete atomic model clarifies dATP selectivity during nucleotide exchange, suggests a role for the b-propellers in assembly, and provides a framework to understand apical procaspase activation.
polyglutamine-induced cell death was dramatically suppressed in flies lacking Dark, the fly homolog of human Apaf-1, a key regulator of apoptosis
structural analysis of Apaf-1 in the auto-inhibited form demonstrates the critical role of ADP [review]
ARK is essential for apoptosis during D. melanogaster development, and for radiation-induced apoptosis. Ark mutant embryos have extra cells, and tissues such as brain lobes and wing discs are enlarged.
identified helical domain I in the nucleotide oligomerization domain as critical for ARK's apoptotic activity.
Daxx-like protein of Drosophila interacts with Dmp53 and affects longevity and Ark mRNA level
Results show that demonstrates that APAF1 expression is regulated by CBX8 in esophageal squamous cell carcinoma cells.
Results strongly suggest that rare mutations in apoptosis-related genes including CASP9, APAF1, and CASP3 contribute to etiology of neural tube defects in Han Chinese population.
Inhibition of TRIAP1 in RPMI8226 cells increased the percentage of apoptotic cells, accompanied by increased expression of APAF1 and Caspase 9, and Caspase 9 and Caspase 3/7 activity.
interactions between endogenous Apaf-1 and DeltaApaf-1 is stronger than its interaction with native exogenous Apaf-1 as indicated by dominant negative effect of DeltaApaf-1 on caspase-3 processing
APAF1 mutations cause recurrent folate-resistant neural tube defects.
Study suggests a potential underlying molecular mechanism of apoptosis inhibition via APAF1 downregulation in human neuroblastoma BE(2)C cells with miRNA36133p overexpression.
Down-regulation of Apaf-1 protein and the overexpression of Cyclin D1 and AQP-5 proteins possibly contribute to an aggressive serous ovarian carcinoma with a high risk of recurrence and poor response to the first-line chemotherapy.
Results suggest that low levels of Apaf-1 as an adaptor protein might be considered as a possible regulatory barrier by which differentiating cells control cell death upon rise in ROS production and cytochrome c release from mitochondria.
APAF-1 was found to be reduced in non-small-cell lung cancer tissue samples along with high expression of miR-484.
miR-300 regulates the cellular sensitivity to ionizing radiation through targeting p53 and apaf1 in lung cancer cells.
we sought to investigate mechanisms mediated by Hsp70 acetylation in relation to apoptotic and autophagic programmed cell death. Upon stress-induced apoptosis, Hsp70 acetylation inhibits apoptotic cell death, mediated by Hsp70 association with apoptotic protease-activating factor (Apaf)-1 and apoptosis-inducing factor (AIF), key modulators of caspase-dependent and -independent apoptotic pathways, respectively
Knockdown of microRNA-27a increased the expression level of Apaf-1, enhancing the formation of Apaf-1-caspase-9 complex and subsequently promoting the TRAIL-induced apoptosis in colorectal cancer stem cells. Findings suggested that knockdown of microRNA-27a in colorectal cancer stem cells by the specific antioligonucleotides was potential to reverse the chemoresistance to TRAIL.
Results indicate that the apoptotic protease-activating factor 1 (Apaf-1) apoptosome activates caspase-9 in part through sequestration of the inhibitory caspase recruitment domains (CARDs) domain.
Authors found significant up-regulation of miR-221 and significant down-regulation of Apaf-1 expression in LSCC tissues compared to normal nearby laryngeal tissues. Significant associations between up-regulated miR-221 and down-regulated Apaf-1 expressions and clinical stage and lymph node (LN) metastasis were found.
A significant correlation between changes in the levels of expression and methylation was detected for the three apoptosis-regulatory genes (APAF1, DAPK1, and BCL2). The results suggest that methylation play an important role in the regulation of the apoptosis system genes in breast cancer.
Primary cells derived from patients with diffuse large B cell lymphomas show membrane raft sequestration of the apoptosome adaptor protein, Apaf-1, which may mediate drug resistance.
Loss of APAF-1 expression is associated with early recurrence in stage I-III colorectal cancer, suggesting that APAF-1 may have clinical value as a predictive marker of early recurrence.
the markers Ets-1 and APAF-1 relative to p53, Ki-67 and PTEN expression in colon adenomas/polyps, were investigated.
Different selenium concentrations had varying effects on BAK1 and APAF1 levels. APAF1 may play an important role in the pathogenesis of KBD
miR21 is transferred from cancer-associated adipocytes (CAAs) and fibroblasts (CAFs) to the cancer cells, where it suppresses ovarian cancer apoptosis and confers chemoresistance by binding to its direct novel target, APAF1.
data collectively demonstrated that Apaf1 is a negative regulator of T cell responses and implicated Apaf1 as a potential target for immunosuppressive drug discovery
miR-183 was induced in protective postconditioning and reduced reperfusion injury of the livers via the targeting of apoptotic signaling. miR-183 mediated the tolerance induced by iPoC in livers via Apaf-1 repressing.
Apaf1's pivotal role during embryonic development as has been demonstrated to be in regulation of neuronal cell death
Inhibition of Caspase-9 restricted, while Apaf-1 promoted, Chlamydia pneumoniae infection in HEp-2, HeLa, and mouse epithelial fibroblast (MEF) cells.
Apaf1 is required for proper cortical neuron differentiation since its deletion specifically impairs axonal outgrowth.
study demonstrates that MMP-3 leads to caspase-9 activation and suggests that this occurs indirectly via a cytosolic protein, possibly involving Apaf-1
results provide evidence that Apaf-1 pharmacological inhibition has therapeutic potential for the treatment of apoptosis-related diseases.
Study reports experimental evidence suggesting the likely participation of the Apaf1 protein in the aggregation of polyQ stretches; Apaf1 may enhance polyglutamine aggregation by reducing the cellular protein levels of available functional Hsp70
miR-23a/b and miR-27a/b are endogenous inhibitory factors of Apaf-1 expression and regulate the sensitivity of neurons to apoptosis.
a role for Apaf1 at the mitochondria
The Apaf-1-independent caspase activation was not inhibited by Bcl-2, and occurred without the release of cytochrome c from mitochondria, suggesting that the mitochondrial pathway was not involved in this death process.
These data are consistent with a model in which alterations of GH signaling and/or insulin sensitivity lead to increased lifespan mediated by decreased renal expression of pro-apoptotic genes.
we have for the first time demonstrated the critical role of Apaf-1 in the regulation of MAP kinases, rective oxygen species and mitochondrial membrane potential in UVC-radiated fibroblasts.
plays a pro-survival role by regulating centrosome morphology and function
Crystal structure of full-length Apaf-1, proper function of Apaf-1 relies on R265 in the vicinity of the bound nucleotide
Ku70/86 binds to the Apaf1 promoter and represses its activity.
Findings suggest that Apaf-1/caspase-9-mediated nonapoptotic caspase signaling is required for the proper neural network formation during olfactory development.
Non-apoptotic cell death of neural progenitor cells may compensate for APAF-1 deficiency in developing central nervous systems.
A drug targeting Apaf-1 allows protection from apoptosis as well as regeneration in the course of inflammation-induced tissue injury
Apaf-1 plays a critical role in apoptosis in a subset of tissues and that both E2F1:p53:Apaf-1-dependent and -independent apoptotic pathways operate downstream of Rb.
Counterpulsation could protect vascular endothelial cells from apoptosis, delaying early atherosclerotic lesions possibly through transcriptional down-regulation of pro-apoptotic gene Apaf-1, and up-regulation of anti-apoptotic gene BIRC2.
This gene encodes a cytoplasmic protein that initiates apoptosis. This protein contains several copies of the WD-40 domain, a caspase recruitment domain (CARD), and an ATPase domain (NB-ARC). Upon binding cytochrome c and dATP, this protein forms an oligomeric apoptosome. The apoptosome binds and cleaves caspase 9 preproprotein, releasing its mature, activated form. Activated caspase 9 stimulates the subsequent caspase cascade that commits the cell to apoptosis. Alternative splicing results in several transcript variants encoding different isoforms.
, Apaf-1 related killer
, Apaf-1-related killer
, apaf1-related killer
, drosophila Apaf-1-related killer
, lethal (2) SH0173
, transcription unit 1
, apoptotic peptidase activating factor 1
, apoptotic protease-activating factor 1-like
, apoptotic protease-activating factor 1
, apoptotic protease activating factor 1
, forebrain overgrowth