Team:Warsaw/Modelling/Gene Networks
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==Simplified description of the cytoplasmatic switch== | ==Simplified description of the cytoplasmatic switch== | ||
- | This simple model is based on kinetic differential equations which are used to describe the kinetics of chemical reactions. We assumed that all cro proteins is already degraded and only AraC and TetR regulate the expression of the proapoptotic proteins. The abbreviations are the same as the picture that depict the regulatory system | + | This simple model is based on kinetic differential equations which are used to describe the kinetics of chemical reactions. We assumed that all cro proteins is already degraded and only AraC and TetR regulate the expression of the proapoptotic proteins. The abbreviations are the same as the picture that depict the regulatory system. |
[[Image:Differential 1.png|thumb|680px|Kinetics of AraC]] | [[Image:Differential 1.png|thumb|680px|Kinetics of AraC]] | ||
[[Image:Differential 2.png|thumb|680px|Kinetics of Bax]] | [[Image:Differential 2.png|thumb|680px|Kinetics of Bax]] | ||
+ | The mechanistic consideration are simple. The repressor protein tightly bind to DNA preventing from initation of transcription. It is assumed that almost all promoters are blocked. Addition of tetracycline or arabinose lead to | ||
+ | dynamic equlibrium. Some protein molecules create complexes with their ligands which are not blocked the transcription. Due to lack of direct interactions between these two proteins regulation of both transcription is independ. To simplify the equations we also assume that concentration of mRNAs is explicite depend on time and there is no implicit variables in the system. The ratio of translation is equal for all trancripts due to usage the same RBS for all of them. | ||
Revision as of 02:56, 22 October 2009
Contents |
Why model?
Model overview
Parameters
Conclusions
Simplified description of the cytoplasmatic switch
This simple model is based on kinetic differential equations which are used to describe the kinetics of chemical reactions. We assumed that all cro proteins is already degraded and only AraC and TetR regulate the expression of the proapoptotic proteins. The abbreviations are the same as the picture that depict the regulatory system.
The mechanistic consideration are simple. The repressor protein tightly bind to DNA preventing from initation of transcription. It is assumed that almost all promoters are blocked. Addition of tetracycline or arabinose lead to dynamic equlibrium. Some protein molecules create complexes with their ligands which are not blocked the transcription. Due to lack of direct interactions between these two proteins regulation of both transcription is independ. To simplify the equations we also assume that concentration of mRNAs is explicite depend on time and there is no implicit variables in the system. The ratio of translation is equal for all trancripts due to usage the same RBS for all of them.