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states using the reduced-order binary decision diagram (ROBDD) algorithm. A steady
state is a network state to which the network returns, i.e. a stable state that is reached
again even after changes or disturbances and does not change. Especially helpful is the
perturbation function in SQUAD, with which one can write one’s own protocol and
define exactly which activation a certain node has at a certain point in time, in order to
map or predict the simulation e.g. according to the experimental data and the mutation
background (administration of a drug, knockouts, activation of receptors). For step c),
there is a good tutorial for SQUAD and an example network (T-helper cell network)
that you can practice with to get started. In addition, you can practice a bioinformatics
in silico simulation on your own by watching our online tutorial (https://www.ncbi.
nlm.nih.gov/pubmed/27077967). Here you will be shown all the necessary steps and
can “recreate” it yourself (scripts for simulation can be found there as well). An alter
native is our own software Jimena, which also has a nice online tutorial (https://www.
bioinfo.biozentrum.uni-wuerzburg.de/computing/jimena_c/).
How Do I Perform Metabolic Modeling of Metabolic Pathways/Fluxes?
It should be noted that one needs as input file for the elementary mode analysis a list of all
enzymes (reversible or irreversible should be decided according to the physiological con
ditions) and a list of all enzyme substrates. Then the given algorithms can calculate all
modes effortlessly. But unfortunately, an enzyme can have more substrates than known in
the KEGG database (https://www.genome.jp/kegg/). So, in addition, one has to consider
biochemical knowledge, literature and databases like the BRENDA database (https://
www.brenda-enzymes.de), which collects very many substrates for an enzyme, along with
information about Michaelis–Menten constant and biochemistry. Finally, metabolic
enzymes without substrate or under special conditions (e.g. without iron) can suddenly
acquire new regulatory functions.
It is interesting to note that dynamic modelling using gene expression data is only an
approximation of the true fluxes, but in practice such gene expression data are much more
likely to be available than the laborious determination of metabolite concentrations.
Dynamic modelling can then also look at true concentrations and kinetics for metabolites,
for example using the software PLAS (Power Law Analysis Software – modelled with
power functions; https://enzymology.fc.ul.pt/software/plas/). In addition, for the calcula
tion of metabolic pathways/fluxes (elementary mode analysis and flux mode calculation)
there are our developed programs Metatool (calculation of all possible metabolic path
ways; the Metatool input files have to be edited exactly, otherwise the simple program
crashes. It is recommended to start with a simple example, see online tutorial, and then
adapt the example file step by step) and YANAsquare (calculation possible for certain situ
ations, e.g. exponential growth with glucose as nutrient source or without oxygen: which
pathways are then active and how strongly, see exercise tasks for elementary mode analy
sis). As a first introduction and good basis for metabolic analysis, the online tutorials for
Metatool (https://www.bioinfo.biozentrum.uni-wuerzburg.de/computing/metatool_4_5/;
19.4 Cellular Communication, Signalling Cascades, Metabolism, Shannon Entropy