Systematic complexity reduction of signaling models and application to a CD95 signaling model for apoptosis.

A major problem when designing mathematical models of biochemical processes to analyze and explain experimental data is choosing the correct degree of model complexity. A common approach to solve this problem is top-down: Initially, complete models including all possible reactions are generated; they are then iteratively reduced to a more manageable size. The reactions to be simplified at each step are often chosen manually since exploration of the full search space seems unfeasible. While such a strategy is sufficient to identify a single, clearly structured reduction of the model, it discards additional information such as whether some model features are essential. In this chapter, we introduce alternate set-based strategies to model reduction that can be employed to exhaustively analyze the complete reduction space of a biochemical model instead of only identifying a single valid reduction

SI: A Guide to Automated Apoptosis Detection

<p>supplementary information of the article:</p> <p>"A Guide to Automated Apoptosis Detection:</p> <p>How to Make Sense of Imaging Flow Cytometry Data"</p> <p>D. Pischel et al., 2018</p

SI: A Guide to Automated Apoptosis Detection

<p>supplementary information of the article:</p> <p>"A Guide to Automated Apoptosis Detection:</p> <p>How to Make Sense of Imaging Flow Cytometry Data"</p> <p>D. Pischel et al., 2018</p

Apoptotic cell death in disease-Current understanding of the NCCD 2023.

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease