Skip to main content

Table 1 Key publications in apoptosis systems modeling

From: System-based approaches as prognostic tools for glioblastoma

YearAuthorMajor findingsRef.
2000Fussenegger et al.Theoretical study on mitochondrial permeabilization induced by BCL-2 family proteins[127]
2004Eissing et al.Theoretical study analysing death receptor-induced apoptosis including bistability analysis[128]
2004Bentele et al.ODE-based modelling of apoptosis signalling supported by quantitative Western blotting[125]
2005Stucki et al.Theoretical study into mitochondrial cytochrome-c and SMAC release on caspase activation[129]
2006Rehm et al.First study that combined single cell imaging and ODE modelling of caspase activation in response to mitochondrial permeabilization (MOMP)[47]
2006Bagci et al. & Legewie et al.Theoretical studies that highlighted positive feedback loops which guarantee bistability subsequent to MOMP and co-operation in Apaf-1 oligomerisation[130, 131]
2007Chen et al.Theoretical study on Bax-activation[132]
2007Lavrik et al.Introduced robustness analysis into the field. Provided structural model of extrinsic apoptosis induced by CD95/Apo-1[133]
2007Eissing et al.Theoretical studies to evaluate robustness of computational models against parameter variations[134, 135]
2008Albeck et al.Combined study employing live cell imaging of caspase activation and MOMP, flow cytometry, immunoblotting and modelling during death receptor-induced apoptosis[126]
2009Zhang et al.Theoretical study into how genotoxic stress proceeds to MOMP and caspase activation[136]
2009Chen et al. & Dussmann et al.Application of stochastic models based on cellular automata (CA) to study Bax activation in mitochondrial membranes during apoptosis[137, 138]
2009 & 2010Rehm et al. & Huber et al.Spatial signal propagation during apoptosis signalling including experimental testing and mathematical modelling using partial differential equations (PDE)[123, 124]
2011Aldridge et al.Combined in silico and wet-lab analyses focussed on TRAIL-induced apoptosis[139]
2011Lau et al.Identification of spatial and temporal aspects of apoptosis signalling[140]
2012Hector et al.Clinical application of caspase modelling to predict recurrence in CRC[13]
2012Lee et al.Combined study employing mathematical modelling and wet-lab validation identifying optimal treatment scheduling for apoptosis re-sensitization[141]
2012Gaudet et al.Comprehensive assessment with sensitivity analyses of the impact of cell-to-cell deviations in protein concentrations on apoptosis dynamics[142]
2012Schleich et al.Combined theoretical and wet-lab analyses into the role of apoptosis activation by caspase-8[143]
2013Lindner et al.Use of BCL-2 systems analysis to predict patient response to chemotherapy in CRC[18]
2013Murphy et al.Use of systems analysis to predict progression-free survival in GBM[17]
2014Kallenberger et al.Combined in silico and wet-lab study into the regulation of apoptosis by caspase-8[144]
2014 & 2015Bertaux et al. & Roux et al.Theoretical study investigating fractional killing in apoptosis[145, 146]
2015 & 2016Zhao et al. & Li et al.Theoretical study into the role played by mutations in apoptosis signalling[147, 148]
2017Salvucci et al.Large scale validation of caspase modelling as independent prognostic biomarker in CRC and refinement of the prognostic power of apoptosis systems models with machine learning[19]
2017Lindner et al.Large scale validation of BCL-2 modelling as independent prognostic biomarker in CRC and analysis of apoptosis systems models in molecular subtypes of CRC[20]
2018Márquez-Jurado et al.Study combining mathematical modelling with experimental microscopy data focussed on the role played by mitochondria in regulating apoptosis[149]
2018Hantusch et al.Regulation of BCL-XL via Bax retrotranslocation[150]