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A key event during apoptosis is mitochondrial outer membrane permeabilization (MOMP), which typically proceeds in a rapid all-or-none fashion. If MOMP occurs only in a subset of mitochondria (minority MOMP), it can be sublethal and contribute to tumorigenesis and cancer progression. Similarly, individual mitochondria escaping widespread MOMP (majority MOMP) can allow cancer cells to recover if apoptosis execution fails. How such heterogeneities in mitochondrial MOMP responsiveness arise within cells is incompletely understood. In particular, whether stochasticity in subcellular protein distributions and interactions across cytosol and mitochondria can realistically contribute to mitochondrial MOMP heterogeneity has not yet been studied. To assess this, we sequentially built and experimentally parameterized a particle-based, cell-sized model including cytosolic and mitochondrial compartments, and that featured a reduced interactome of MCL-1, BAK and tBID. High-performance computing enabled cell-scale simulations of protein distributions and interactions to understand how and under which conditions stochasticity could contribute to heterogeneity in MOMP susceptibility. Our results show that stochastic effects strongly predispose sub-pools of fragmented mitochondria to MOMP under low apoptotic stress. At higher apoptotic stress, fractions of small mitochondria were more likely to escape MOMP than large mitochondria. Retrospective quantification of mitochondrial sizes in experimental scenarios of minority and majority MOMP confirmed these findings. We therefore conclude that stochasticity substantially contributes to enabling small or fragmented mitochondria to undergo MOMP in minority MOMP scenarios and to escape MOMP in majority MOMP scenarios.", "issn" : "20414889", "refid" : "Geiger2025", "doi" : "10.1038/s41419-025-08258-9", "bibtexKey": "geiger2025stochasticity" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/25412e286ad50be992694b6b4887dff31/simtechpuma", "tags" : [ "PN2","PN2-7","PN5","EXC2075","PN5-6(II)","selected" ], "intraHash" : "5412e286ad50be992694b6b4887dff31", "interHash" : "5a4875d858175206d6f85d84a00a0456", "label" : "Uncertainty-Aware Surrogate-based Amortized Bayesian Inference for Computationally Expensive Models", "user" : "simtechpuma", "description" : "", "date" : "2026-02-16 15:04:58", "changeDate" : "2026-02-16 15:04:58", "count" : 6, "pub-type": "article", "journal": "Transactions in Machine Learning Research", "year": "2026", "url": 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A key event during apoptosis is mitochondrial outer membrane permeabilization (MOMP), which typically proceeds in a rapid all-or-none fashion. If MOMP occurs only in a subset of mitochondria (minority MOMP), it can be sublethal and contribute to tumorigenesis and cancer progression. Similarly, individual mitochondria escaping widespread MOMP (majority MOMP) can allow cancer cells to recover if apoptosis execution fails. How such heterogeneities in mitochondrial MOMP responsiveness arise within cells is incompletely understood. In particular, whether stochasticity in subcellular protein distributions and interactions across cytosol and mitochondria can realistically contribute to mitochondrial MOMP heterogeneity has not yet been studied. To assess this, we sequentially built and experimentally parameterized a particle-based, cell-sized model including cytosolic and mitochondrial compartments, and that featured a reduced interactome of MCL-1, BAK and tBID. High-performance computing enabled cell-scale simulations of protein distributions and interactions to understand how and under which conditions stochasticity could contribute to heterogeneity in MOMP susceptibility. Our results show that stochastic effects strongly predispose sub-pools of fragmented mitochondria to MOMP under low apoptotic stress. At higher apoptotic stress, fractions of small mitochondria were more likely to escape MOMP than large mitochondria. Retrospective quantification of mitochondrial sizes in experimental scenarios of minority and majority MOMP confirmed these findings. 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Schmid","Tobias B. Beigl","Alexandra Mack","Daniela S. Maichl","Kai Cao","Beate Budai","Gavin Fullstone","Roland E. Kontermann","Thomas E. Mürdter","Stephen W. G. Tait","Cathrin Hagenlocher","Nadine Pollak","Peter Scheurich","Markus Rehm" ], "authors": [ {"first" : "Daniela", "last" : "Stöhr"}, {"first" : "Jens O.", "last" : "Schmid"}, {"first" : "Tobias B.", "last" : "Beigl"}, {"first" : "Alexandra", "last" : "Mack"}, {"first" : "Daniela S.", "last" : "Maichl"}, {"first" : "Kai", "last" : "Cao"}, {"first" : "Beate", "last" : "Budai"}, {"first" : "Gavin", "last" : "Fullstone"}, {"first" : "Roland E.", "last" : "Kontermann"}, {"first" : "Thomas E.", "last" : "Mürdter"}, {"first" : "Stephen W. G.", "last" : "Tait"}, {"first" : "Cathrin", "last" : "Hagenlocher"}, {"first" : "Nadine", "last" : "Pollak"}, {"first" : "Peter", "last" : "Scheurich"}, {"first" : "Markus", "last" : "Rehm"} ], "issn" : "14765403", "refid" : "Stöhr2020", "doi" : "10.1038/s41418-020-0559-3", "bibtexKey": "stohr2020stressinduced" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/26e3ce7087c12ef183e2bd84a070b335e/pumaizi", "tags" : [ "myown","pn2","simtech","izi","EXC2075","2020","morrison" ], "intraHash" : "6e3ce7087c12ef183e2bd84a070b335e", "interHash" : "51c30b9ac193efb587e30fa6347fc318", "label" : "Convergence of pathway analysis and pattern recognition predicts sensitization to latest generation TRAIL therapeutics by IAP antagonism", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 10, "pub-type": "article", "journal": "Cell Death & Differentiation 2020","publisher":"Nature Publishing Group", "year": "2020", "url": "https://www.nature.com/articles/s41418-020-0512-5", "author": [ "Vesna Vetma","Cristiano Guttà","Nathalie Peters","Christian Praetorius","Meike Hutt","Oliver Seifert","Friedegund Meier","Roland Kontermann","Dagmar Kulms","Markus Rehm" ], "authors": [ {"first" : "Vesna", "last" : "Vetma"}, {"first" : "Cristiano", "last" : "Guttà"}, {"first" : "Nathalie", "last" : "Peters"}, {"first" : "Christian", "last" : "Praetorius"}, {"first" : "Meike", "last" : "Hutt"}, {"first" : "Oliver", "last" : "Seifert"}, {"first" : "Friedegund", "last" : "Meier"}, {"first" : "Roland", "last" : "Kontermann"}, {"first" : "Dagmar", "last" : "Kulms"}, {"first" : "Markus", "last" : "Rehm"} ], "pages": "1--16", "issn" : "1476-5403", "doi" : "10.1038/s41418-020-0512-5", "bibtexKey": "Vetma2020" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2037710f5d73ec3084fa674b1d8fbc113/pumaizi", "tags" : [ "myown","pn2","simtech","izi","EXC2075","2020","morrison" ], "intraHash" : "037710f5d73ec3084fa674b1d8fbc113", "interHash" : "67fadc9559cbceec954c3c00a2c2bcba", "label" : "Low expression of pro-apoptotic proteins Bax, Bak and Smac indicates prolonged progression-free survival in chemotherapy-treated metastatic melanoma", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 8, "pub-type": "article", "journal": "Cell Death & Disease","publisher":"Nature Publishing Group", "year": "2020", "url": "http://www.nature.com/articles/s41419-020-2309-3", "author": [ "Cristiano Guttà","Arman Rahman","Claudia Aura","Peter Dynoodt","Emilie M. Charles","Elodie Hirschenhahn","Jesuchristopher Joseph","Jasper Wouters","Ciaran de Chaumont","Mairin Rafferty","Madhuri Warren","Joost J. van den Oord","William M. Gallagher","Markus Rehm" ], "authors": [ {"first" : "Cristiano", "last" : "Guttà"}, {"first" : "Arman", "last" : "Rahman"}, {"first" : "Claudia", "last" : "Aura"}, {"first" : "Peter", "last" : "Dynoodt"}, {"first" : "Emilie M.", "last" : "Charles"}, {"first" : "Elodie", "last" : "Hirschenhahn"}, {"first" : "Jesuchristopher", "last" : "Joseph"}, {"first" : "Jasper", "last" : "Wouters"}, {"first" : "Ciaran", "last" : "de Chaumont"}, {"first" : "Mairin", "last" : "Rafferty"}, {"first" : "Madhuri", "last" : "Warren"}, {"first" : "Joost J.", "last" : "van den Oord"}, {"first" : "William M.", "last" : "Gallagher"}, {"first" : "Markus", "last" : "Rehm"} ], "volume": "11","number": "2","pages": "124","abstract": "Despite the introduction of novel targeted therapies, chemotherapy still remains the primary treatment for metastatic melanoma in poorly funded healthcare environments or in case of disease relapse, with no reliable molecular markers for progression-free survival (PFS) available. As chemotherapy primarily eliminates cancer cells by apoptosis, we here evaluated if the expression of key apoptosis regulators (Bax, Bak, Bcl-2, Bcl-xL, Smac, Procaspase-9, Apaf-1, Procaspase-3 and XIAP) allows prognosticating PFS in stage III/IV melanoma patients. Following antibody validation, marker expression was determined by automated and manual scoring of immunohistochemically stained tissue microarrays (TMAs) constructed from treatment-naive metastatic melanoma biopsies. Interestingly and counter-intuitively, low expression of the pro-apoptotic proteins Bax, Bak and Smac indicated better prognosis (log-rank p\u2009\\textless\u20090.0001, p\u2009=\u20090.0301 and p\u2009=\u20090.0227 for automated and p\u2009=\u20090.0422, p\u2009=\u20090.0410 and p\u2009=\u20090.0073 for manual scoring). These findings were independently validated in the cancer genome atlas (TCGA) metastatic melanoma cohort (TCGA-SKCM) at transcript level (log-rank p\u2009=\u20090.0004, p\u2009=\u20090.0104 and p\u2009=\u20090.0377). Taking expression heterogeneity between the markers in individual tumour samples into account allowed defining combinatorial Bax, Bak, Smac signatures that were associated with significantly increased PFS (p\u2009=\u20090.0002 and p\u2009=\u20090.0028 at protein and transcript level, respectively). Furthermore, combined low expression of Bax, Bak and Smac allowed predicting prolonged PFS (\\textgreater\u200912 months) on a case-by-case basis (area under the receiver operating characteristic curve (ROC AUC)\u2009=\u20090.79). Taken together, our results therefore suggest that Bax, Bak and Smac jointly define a signature with potential clinical utility in chemotherapy-treated metastatic melanoma.", "file" : ":C$\\backslash$:/Users/cgu/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Guttà et al. - 2020 - Low expression of pro-apoptotic proteins Bax, Bak and Smac indicates prolonged progression-free survival in chemot.pdf:pdf", "issn" : "2041-4889", "doi" : "10.1038/s41419-020-2309-3", "bibtexKey": "Gutta2020" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/2c7705e67a91e5be1873cf1aa4dc28045/pumaizi", "tags" : [ "pn2","simtech","izi","2022","EXC2075","hausser","morrison" ], "intraHash" : "c7705e67a91e5be1873cf1aa4dc28045", "interHash" : "040e11e469229e3642b9b49a135a599c", "label" : "ER stress-induced cell death proceeds independently of the TRAIL-R2 signaling axis in pancreatic β cells", "user" : "pumaizi", "description" : "ER stress-induced cell death proceeds independently of the TRAIL-R2 signaling axis in pancreatic β cells | Cell Death Discovery", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 7, "pub-type": "article", "journal": "Cell Death Discovery", "year": "2022", "url": "https://doi.org/10.1038/s41420-022-00830-y", "author": [ "Cathrin Hagenlocher","Robin Siebert","Bruno Taschke","Senait Wieske","Angelika Hausser","Markus Rehm" ], "authors": [ {"first" : "Cathrin", "last" : "Hagenlocher"}, {"first" : "Robin", "last" : "Siebert"}, {"first" : "Bruno", "last" : "Taschke"}, {"first" : "Senait", "last" : "Wieske"}, {"first" : "Angelika", "last" : "Hausser"}, {"first" : "Markus", "last" : "Rehm"} ], "volume": "8","number": "1","pages": "34", "issn" : "2058-7716", "doi" : "10.1038/s41420-022-00830-y", "bibtexKey": "Hagenlocher2022" } , { "type" : "Publication", "id" : "https://puma.ub.uni-stuttgart.de/bibtex/278a66607436137f1e02612815bdb384f/pumaizi", "tags" : [ "PN2","EXC2075" ], "intraHash" : "78a66607436137f1e02612815bdb384f", "interHash" : "46e77ba52c4a050484a3d5cb40a498ef", "label" : "Marizomib sensitizes primary glioma cells to apoptosis induced by a latest-generation TRAIL receptor agonist", "user" : "pumaizi", "description" : "", "date" : "2025-10-17 10:53:57", "changeDate" : "2025-10-17 10:53:57", "count" : 9, "pub-type": "article", "journal": "Cell Death & Disease","publisher":"Nature Publishing Group", "year": "2021", "url": "http://www.nature.com/articles/s41419-021-03927-x", "author": [ "Chiara Boccellato","Emily Kolbe","Nathalie Peters","Viktorija Juric","Gavin Fullstone","Maïté Verreault","Ahmed Idbaih","Martine L. 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