SGP2024 - Apoptosis_AgNPs
Ontology highlight
ABSTRACT:
SUBMITTER: 
Seung-Geun Park
PROVIDER: MODEL2412210001 | BioModels | 2025-09-08
REPOSITORIES: BioModels
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| MODEL2412210001?filename=COPASI_AgNPs_model.cps | Other | |||
| MODEL2412210001?filename=CellDesigner_AgNPs_model_SBML.xml | Xml |
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Similar Datasets
Project description:Pharmacological intervention of redox balance in cancer cells often results in oxidative stress-mediated apoptosis, attracting much attention for the development of a new generation of targeted therapy in cancer. However, little is known about mechanisms underlying the conversion from oxidative signaling to downstream activities leading cells to death. We here report a systematic detection of transcriptome changes in response to oxidative signals generated in leukemia cells upon fenretinide treatment, implicating the occurrence of numerous stress-responsive events during the fenretinide induced apoptosis, such as redox response, endoplasmic reticulum stress/unfolded protein response, translational repression and proteasome activation. Moreover, the configuration of these relevant events is primarily orchestrated by stress responsive transcription factors, as typically highlighted by NF-E2-related factor-2 (NRF2) and heat shock factor 1 (HSF1). Several lines of evidence suggest that the coordinated regulation of these transcription factors and thus their downstream genes are involved in converting oxidative signaling into downstream stress-responsive events regulating pro-apoptotic and apoptotic activities at the temporal and spatial levels, typifying oxidative stress-mediated programmed death rather than survival in cancer cells. This study provides a roadmap for understanding oxidative stress-mediated apoptosis in cancer cells, which may be further developed into more sophisticated therapeutic protocols, as implicated by synergistic induction of cell apoptosis using proteasome inhibitors with fenretinide. Time-series experiment, fenretinide treated NB4 cells at 19 time points (i.e., 0.25, 0.5, 1, 2, 4, 6, 8, 10, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54 and 60 hours) and untreated NB4 cells at 4 time points (i.e., 0, 8, 12 and 15 hours).
2010-05-05 | E-GEOD-16578 | biostudies-arrayexpress
Project description:Pharmacological intervention of redox balance in cancer cells often results in oxidative stress-mediated apoptosis, attracting much attention for the development of a new generation of targeted therapy in cancer. However, little is known about mechanisms underlying the conversion from oxidative signaling to downstream activities leading cells to death. We here report a systematic detection of transcriptome changes in response to oxidative signals generated in leukemia cells upon fenretinide treatment, implicating the occurrence of numerous stress-responsive events during the fenretinide induced apoptosis, such as redox response, endoplasmic reticulum stress/unfolded protein response, translational repression and proteasome activation. Moreover, the configuration of these relevant events is primarily orchestrated by stress responsive transcription factors, as typically highlighted by NF-E2-related factor-2 (NRF2) and heat shock factor 1 (HSF1). Several lines of evidence suggest that the coordinated regulation of these transcription factors and thus their downstream genes are involved in converting oxidative signaling into downstream stress-responsive events regulating pro-apoptotic and apoptotic activities at the temporal and spatial levels, typifying oxidative stress-mediated programmed death rather than survival in cancer cells. This study provides a roadmap for understanding oxidative stress-mediated apoptosis in cancer cells, which may be further developed into more sophisticated therapeutic protocols, as implicated by synergistic induction of cell apoptosis using proteasome inhibitors with fenretinide.
2009-09-15 | GSE16578 | GEO
Project description:This model is from the article:
Systems biology analysis of programmed cell death
Shani Bialik, Einat Zalckvar, Yaara Ber, Assaf D. Rubinstein, Adi Kimchi Trends in Biochemical Sciences
Volume 35, Issue 10, 556-564, 27 May 2010 20537543
,
Abstract:
Systems biology, a combined computational and experimental approach to analyzing complex biological systems, has recently been applied to understanding the pathways that regulate programmed cell death. This approach has become especially crucial because recent advances have resulted in an expanded view of the network, to include not just a single death module (apoptosis) but multiple death programs, including programmed necrosis and autophagic cell death. Current research directions in the systems biology field range from quantitative analysis of subprocesses of individual death pathways to the study of interconnectivity among the various death modules of the larger network. These initial studies have provided great advances in our understanding of programmed cell death and have important clinical implications for drug target research.
Brief Note about the model:
This model is an export of 26 SPIKE
Apoptosis Networks to SBML format.
This is a pathway model (not quantitative model) of Apoptosis.
Apoptosis, or type I cell death, is a form of programmed cell death
characterized by fragmentation of the cytoplasm and nucleus, chromatin
condensation and fragmentation, cytoskeletal collapse, membrane
blebbing, and finally, disintegration of the cell into apoptotic
bodies, which are engulfed by adjacent cells, thereby avoiding an
inflammatory response. It serves to model tissues during embryonic
development, to regulate cell number by eliminating excess cells, and
to remove damaged, mutated or infected cells. Defective or excessive
apoptosis can lead to cancer or autoimmune and degenerative diseases,
respectively. Apoptosis is executed by a family of cysteine proteases,
the caspases, which function in a proteolytic cascade that is
initiated by either the intrinsic mitochondrial-based pathway leading
to apoptosome formation, or the extrinsic pathway, which involves
activation of death receptors by their extracellular ligands to form
the DISC. The most distal caspases, known as the executioner caspases,
cleave numerous cellular substrates, thereby leading to specific
dismantling of the cell. Apoptosis is regulated by multiple proteins
at several levels, including the Bcl-2 family, which regulate the
release of apoptogenic factors from the mitochondria, and the IAP
family, which regulate caspase activity, and is countered by survival
signals eminating from the NF-kB signaling pathway. Although most of
the regulation occurs at the post-translational level, involving
protein-protein interactions, proteolysis, changes in subcellular
localization and phosphorylation, transcriptional control, such as by
p53, can also modulate the expression levels of several key apoptotic
proteins.
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.
.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1107050000 | BioModels
Project description:Programmed cell death plays a vital role in shaping limb morphology in amniotes. BMP signaling has been shown to be essential for inducing interdigital cell death, but its relationship with reactive oxygen species (ROS) production, a known driver of this process, remains unclear. Here, we explore the molecular mechanisms by which BMP signaling regulates ROS production and cell death in the interdigital regions of chicken hindlimbs. To identify the ROS-producing cascade genes regulated by BMP signaling, we performed RNA-Seq of the interdigital region with PBS or Noggin bead implantation in chicken hindlimb buds. Subsequently, we performed RNA-seq of the interdigital region from stage 30 to stage 31 chicken hindlimb buds to analyze temporal expression changes of ROS-related genes during the normal progression of interdigital cell death in chicken hindlimbs. This study provides new insights into the ROS-mediated mechanisms of BMP-driven programmed cell death, highlighting the coordinated regulation of ROS generation and scavenging in limb morphogenesis.
2025-12-08 | GSE279142 | GEO
Project description:Programmed cell death plays a vital role in shaping limb morphology in amniotes. BMP signaling has been shown to be essential for inducing interdigital cell death, but its relationship with reactive oxygen species (ROS) production, a known driver of this process, remains unclear. Here, we explore the molecular mechanisms by which BMP signaling regulates ROS production and cell death in the interdigital regions of chicken hindlimbs. To identify the ROS-producing cascade genes regulated by BMP signaling, we performed RNA-Seq of the interdigital region with PBS or Noggin bead implantation in chicken hindlimb buds. Subsequently, we performed RNA-seq of the interdigital region from stage 30 to stage 31 chicken hindlimb buds to analyze temporal expression changes of ROS-related genes during the normal progression of interdigital cell death in chicken hindlimbs. This study provides new insights into the ROS-mediated mechanisms of BMP-driven programmed cell death, highlighting the coordinated regulation of ROS generation and scavenging in limb morphogenesis.
2025-12-08 | GSE279141 | GEO
Project description:Cells are constantly exposed to stress. Most of those stresses do not necessarily cause cell death or visible damage. The present study explores the way the immune system responds to such sub lethal stressed cells. HF cells were exposed to sublethal oxidative stress or mock treated with PBS and after removal of the stressor, HF were incubated with/wthout monocytes for 24h and gene expression was evaluated.
2011-12-01 | E-GEOD-33631 | biostudies-arrayexpress
Project description:Oxygen-glucose deprivation (OGD) is a cellular phenomenon consistently observed upon occurrence of ischemic stroke which eventually results in neuronal death. Neuronal cell death after ischemia takes place via two distinct processes, necrosis and apoptosis. Apoptosis, programmed cell death, is denoted by chromatin condensation, nuclear blebbing, cellular shrinkage, and DNA fragmentation. Unlike apoptosis, cellular swelling and lysis is suggestive of necrosis. However, these two processes are related not only to the severity but also to the duration of ischemia.
2013-12-31 | GSE23158 | GEO
Project description:Cells are constantly exposed to stress. Most of those stresses do not necessarily cause cell death or visible damage. The present study explores the way the immune system responds to such sub lethal stressed cells.
2011-12-01 | GSE33631 | GEO
Project description:Aging was long assumed to be a passive and stochastic process caused by random damage accumulation, however，such theories fail to explain the program-like features of the aging process. Measuring the aging process in C. elegans at individual level provides an opportunity to analyze both the programmed (age-related changes at population level) and stochastic (inter-individual differences in isogenic population) components during the aging process. Here, we performed quantitative proteomic analyses on more than 150 worm individuals of different ages and aged individuals with different mobility. The analysis of inter-individual variations helps dissect the programmed and stochastic components during the aging process, and key proteins underlying the lifespan plasticity among the genetically identical worm individuals. Using a high temporal resolution single worm proteomic landscape, we found that the aging process was non-linearly progressed, with each stage marked by distinct age-related changes. The fast-aging individuals are depleted with such secreted proteins and over-activation of lysosome degradation processes, providing a first molecular link for the programmed enhanced offspring growth and death of the parent individual. This mechanistic link indicates that programmed events at least in part explain the heterogeneity of adult aging.
2023-11-14 | PXD039330 | Pride
Project description:Oxygen-glucose deprivation (OGD) is a cellular phenomenon consistently observed upon occurrence of ischemic stroke which eventually results in neuronal death. Neuronal cell death after ischemia takes place via two distinct processes, necrosis and apoptosis. Apoptosis, programmed cell death, is denoted by chromatin condensation, nuclear blebbing, cellular shrinkage, and DNA fragmentation. Unlike apoptosis, cellular swelling and lysis is suggestive of necrosis. However, these two processes are related not only to the severity but also to the duration of ischemia. Microarray analysis was carried out using 20 Illumina mouse Ref8V1.1 genechip arrays. The assignment of the arrays was as follows: Controls (n=5); exposure to OGD for 10min, 5h, 8h, 15h and 24 h (n=3 respectively).
2013-12-31 | E-GEOD-23158 | biostudies-arrayexpress