Jun Cui
Nanjing University
7 Papers
85 Citations
Jun Cui is an academic researcher from Nanjing University. The author has contributed to research in topics: Proinflammatory cytokine & Granzyme. The author has an hindex of 5, co-authored 7 publications.
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Papers
Induction of Apoptosis in Mouse Liver by Microcystin-LR A Combined Transcriptomic, Proteomic, And Simulation Strategy
TL;DR: It is indicated that MC-LR exposure can cause apoptosis in mouse liver and revealed two independent pathways playing a major regulatory role in MC- LR-induced apoptosis, thereby contributing to a better understanding of the hepatotoxicity and the tumor-promoting mechanisms of MCs.
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Robustness analysis identifies the plausible model of the Bcl-2 apoptotic switch.
TL;DR: By investigating the robustness of other important features of the Bcl‐2 apoptotic switch (including low Bax basal activation, inhibitory role of anti‐apoptotic proteins and insensitivity to small perturbations) the direct activation model was further supported.
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Expression modulation of multiple cytokines in vivo by cyanobacteria blooms extract from taihu lake, China
TL;DR: In vivo data on the immune disorder caused by crude microcystin (MC) extract of cyanobacteria blooms collected from Taihu Lake, China with respect to cytokine mRNA levels are reported and a mathematical model developed to simulate the interaction of T helper cell subsets and related cytokines proved to be a good approach to study the kinetics of the interaction between cells and cytokines in microcyStin immunosuppression.
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Modelling of the mitochondrial apoptosis network
TL;DR: In this paper, an experimental observation-based computer simulation of the regulatory network of mitochondrial apoptosis is performed, and dynamical understandings of various apoptosis-related proteins, including cytochrome c (cyt c) release and caspase activation are obtained.
4
Evaluation of the Function of the Granzyme-Mediated Antiviral System through a Mathematical Model.
TL;DR: A hypothesis is brought forward that most of these oscillations in the gzm-mediated antiviral system may allow ancillary immune responses to effectively suppress a virus as it oscillates through a minimum level.