2015
DOI: 10.1387/ijdb.150047dd
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Apaf1 in embryonic development - shaping life by death, and more

Abstract: Apaf1 has been studied hitherto for its key role in regulating the formation of the apoptotic core machinery, the apoptosome, to induce programmed cell death. Apaf1 involvement in orchestrating this process during embryonic development has been widely documented and constitutes a breakthrough in developmental biology. In this review, we aim to highlight the origin of Apaf1 discoveries and how findings, mainly based on the analysis of knock-out mouse models, have led us to consider Apaf1 as a master player in f… Show more

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Cited by 8 publications
(9 citation statements)
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References 55 publications
(56 reference statements)
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“…Consistently, apart from its canonical role in cell death, it was recently shown that Apaf1 is necessary for other cellular processes, including mitosis, migration, synaptogenesis, and neuronal survival (Ferraro et al, ). For example, neurons lacking Apaf1 exhibit impaired axonal outgrowth, caused by abnormal centrosome organization and alteration of signaling molecules important for axonal extension, including the glycogen synthase kinase‐3b and collapsing‐response mediator protein‐2 (De Zio, Maiani, & Cecconi, ). Apaf1‐deficient mice show hyper proliferation of embryonic NSPCs and decreased apoptosis in the brain, resulting in perinatal lethality (H. Yoshida et al, ).…”
Section: Discussionmentioning
confidence: 99%
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“…Consistently, apart from its canonical role in cell death, it was recently shown that Apaf1 is necessary for other cellular processes, including mitosis, migration, synaptogenesis, and neuronal survival (Ferraro et al, ). For example, neurons lacking Apaf1 exhibit impaired axonal outgrowth, caused by abnormal centrosome organization and alteration of signaling molecules important for axonal extension, including the glycogen synthase kinase‐3b and collapsing‐response mediator protein‐2 (De Zio, Maiani, & Cecconi, ). Apaf1‐deficient mice show hyper proliferation of embryonic NSPCs and decreased apoptosis in the brain, resulting in perinatal lethality (H. Yoshida et al, ).…”
Section: Discussionmentioning
confidence: 99%
“…and collapsing-response mediator protein-2 (De Zio, Maiani, & Cecconi, 2015). Apaf1-deficient mice show hyper proliferation of embryonic NSPCs and decreased apoptosis in the brain, resulting in perinatal lethality (H. Yoshida et al, 1998).…”
Section: Discussionmentioning
confidence: 99%
“…APAF1 serves a critical role as a regulator of the mitochondrial apoptotic signaling pathway, inducing cell apoptosis by binding with cytochrome C and activating caspase-9 in the cytosol ( 21 ). Previous studies have demonstrated that APAF1 functions as a tumor suppressor by interacting with various miRNAs ( 40 42 ).…”
Section: Discussionmentioning
confidence: 99%
“…Apoptotic protease activating factor 1 (APAF1) is a critical component of the apoptosome and previous studies have demonstrated that it may be activated by various cellular stimuli, including DNA damage and oncogene activation ( 20 , 21 ). APAF1 inactivation is a common event in human tumors, which suggests that it may serve as a tumor suppressor in healthy individuals ( 22 ).…”
Section: Introductionmentioning
confidence: 99%
“…PMAIP1 is a gene which promotes activation of caspases and apoptosis by altering the mitochondrial membrane and efflux of apoptogenic proteins. Apoptotic peptidase activating factor 1 (Apaf-1) is an important regulator of the mitochondrial apoptotic pathway to induce programmed cell death [ 37 , 38 ]. In the present study, Bcl-2 , an anti-apoptotic member of the Bcl-2 family, was up-regulated.…”
Section: Discussionmentioning
confidence: 99%