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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.
Daxx (show DAXX Proteins)-like protein of Drosophila interacts with Dmp53 and affects longevity and Ark mRNA level
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 (show ROS1 Proteins) production and cytochrome c (show CYCS Proteins) release from mitochondria.
APAF-1 was found to be reduced in non-small-cell lung cancer tissue samples along with high expression of miR (show MLXIP Proteins)-484.
miR (show MLXIP Proteins)-300 regulates the cellular sensitivity to ionizing radiation through targeting p53 (show TP53 Proteins) and apaf1 in lung cancer cells.
we sought to investigate mechanisms mediated by Hsp70 (show HSP70 Proteins) acetylation in relation to apoptotic and autophagic programmed cell death. Upon stress-induced apoptosis, Hsp70 (show HSP70 Proteins) acetylation inhibits apoptotic cell death, mediated by Hsp70 (show HSP70 Proteins) association with apoptotic protease-activating factor (Apaf)-1 and apoptosis-inducing factor (AIF (show AIFM1 Proteins)), key modulators of caspase (show CASP3 Proteins)-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 (show CASP9 Proteins) 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 (show CASP9 Proteins) in part through sequestration of the inhibitory caspase (show CASP3 Proteins) recruitment domains (CARDs) domain.
Authors found significant up-regulation of miR (show MLXIP Proteins)-221 and significant down-regulation of Apaf-1 expression in LSCC tissues compared to normal nearby laryngeal tissues. Significant associations between up-regulated miR (show MLXIP Proteins)-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 (show DAPK1 Proteins), and BCL2 (show BCL2 Proteins)). 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.
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 (show MLXIP Proteins)-183 was induced in protective postconditioning and reduced reperfusion injury of the livers via the targeting of apoptotic signaling. miR (show MLXIP Proteins)-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 (show MMP3 Proteins) leads to caspase-9 (show CASP9 Proteins) 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 (show HSP70 Proteins)
miR (show MLXIP Proteins)-23a/b and miR (show MLXIP Proteins)-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
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 (show BIRC2 Proteins).
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