Time filter

Source Type

Nishi-Tokyo-shi, Japan

Shiraishi T.,Sony | Matsuyama S.,Sony Corporation | Kitano H.,Sony | Kitano H.,The Systems Biology Institute | Kitano H.,Okinawa Institute of Science and Technology
PLoS Computational Biology | Year: 2010

Protein-protein interaction and gene regulatory networks are likely to be locked in a state corresponding to a disease by the behavior of one or more bistable circuits exhibiting switch-like behavior. Sets of genes could be over-expressed or repressed when anomalies due to disease appear, and the circuits responsible for this over- or under-expression might persist for as long as the disease state continues. This paper shows how a large-scale analysis of network bistability for various human cancers can identify genes that can potentially serve as drug targets or diagnosis biomarkers. © 2010 Shiraishi et al. Source

Crespo I.,University of Luxembourg | Roomp K.,University of Luxembourg | Jurkowski W.,University of Luxembourg | Kitano H.,The Systems Biology Institute | del Sol A.,University of Luxembourg
BMC Systems Biology | Year: 2012

Background: The activation of immune cells in the brain is believed to be one of the earliest events in prion disease development, where misfolded PrionSc protein deposits are thought to act as irritants leading to a series of events that culminate in neuronal cell dysfunction and death. The role of these events in prion disease though is still a matter of debate. To elucidate the mechanisms leading from abnormal protein deposition to neuronal injury, we have performed a detailed network analysis of genes differentially expressed in several mouse prion models.Results: We found a master regulatory core of genes related to immune response controlling other genes involved in prion protein replication and accumulation, and neuronal cell death. This regulatory core determines the existence of two stable states that are consistent with the transcriptome analysis comparing prion infected versus uninfected mouse brain. An in silico perturbation analysis demonstrates that core genes are individually capable of triggering the transition and that the network remains locked once the diseased state is reached.Conclusions: We hypothesize that this locking may be the cause of the sustained immune response observed in prion disease. Our analysis supports the hypothesis that sustained brain inflammation is the main pathogenic process leading to neuronal dysfunction and loss, which, in turn, leads to clinical symptoms in prion disease. © 2012 Crespo et al.; licensee BioMed Central Ltd. Source

Okinawa Institute of Science, Technology and The Systems Biology Institute | Date: 2013-07-11

A simulation system includes an interface component connected to a public or shared network that has less restrictive access than networks inside the firewall, generating a simulation job and registering the simulation job in a database, a job control component accessing said database to retrieve the simulation job and scheduling the simulation job for execution, and a simulation execution component receiving the simulation job from the job control component, creating executable codes for numerical and parallel computing algorithms and distributing computing processes to multiple computers to execute the simulation job.

The Systems Biology Institute, Okinawa Institute of Science and Technology | Date: 2011-03-31

The present invention sets, for each cells or each condition, a production output of the cells or the biomass based on the measured data and a variable indicating an extent of variation of the production output, calculates a variable range of the production output and the variable in case of combining the multiple cells or conditions based on the production output and the variable set, and calculates an optimum combination within the variable range by using an optimization method.

Okinawa Institute of Science, Technology and The Systems Biology Institute | Date: 2013-06-13

The present invention acquires compound structure data and candidate protein structure data on a candidate protein serving as a candidate for interaction with the compound. The present invention calculates a binding strength between the candidate protein and the compound using a docking simulation method, determines a predicted binding strength corresponding to the binding strength predicted by making a comprehensive evaluation of the binding strength, and determines a predicted protein corresponding to the candidate protein predicted to interact with the compound. The present invention calculates an interaction strength using a binding strength simulation method and determines a predicted interaction strength corresponding to the interaction strength predicted by making the comprehensive evaluation of the interaction strength.

Discover hidden collaborations