Difference between revisions of "Comparison of gene essentiality in genome-wide metabolic models of T. brucei and liver cells"

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(New page: {{Projectproposal |Contact person=Jurgen Haanstra |Master areas=Systems Biology, Bioinformatics |Fulfilled=No }} Trypanosoma brucei is the causative agent of African Sleeping Sickness and ...)
 
 
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|Master areas=Systems Biology, Bioinformatics
 
 
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Trypanosoma brucei is the causative agent of African Sleeping Sickness and the parasite is transmitted by tsetse flies to the bloodstream of mammals. Inside the mammalian host, glycolysis is essential for T. brucei and is therefore is a putative target for antitrypanosomal drugs. Other metabolic pathways may also be potential target pathways. But drugs used inside infected humans can affect a similar metabolic step in human cells. To predict which targets in metabolism may be selective we should compare the metabolic pathways in T. brucei and relevant human cells.   
 
Trypanosoma brucei is the causative agent of African Sleeping Sickness and the parasite is transmitted by tsetse flies to the bloodstream of mammals. Inside the mammalian host, glycolysis is essential for T. brucei and is therefore is a putative target for antitrypanosomal drugs. Other metabolic pathways may also be potential target pathways. But drugs used inside infected humans can affect a similar metabolic step in human cells. To predict which targets in metabolism may be selective we should compare the metabolic pathways in T. brucei and relevant human cells.   
  
 
A genome-based metabolic map is available for both T. brucei and the human genome. For a relevant comparison, these genome-wide models should be adjusted with gene expression data to a restricted version for the bloodstream T. brucei (the clinically relevant lifecycle stage) and a liver-restricted version of the human metabolic model. These models will then be compared to elucidate differences in essentiality of metabolic genes for relevant metabolic fluxes (ATP production flux, cofactor production fluxes)
 
A genome-based metabolic map is available for both T. brucei and the human genome. For a relevant comparison, these genome-wide models should be adjusted with gene expression data to a restricted version for the bloodstream T. brucei (the clinically relevant lifecycle stage) and a liver-restricted version of the human metabolic model. These models will then be compared to elucidate differences in essentiality of metabolic genes for relevant metabolic fluxes (ATP production flux, cofactor production fluxes)

Latest revision as of 10:01, 24 August 2016


About Comparison of gene essentiality in genome-wide metabolic models of T. brucei and liver cells


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|free text=}} Trypanosoma brucei is the causative agent of African Sleeping Sickness and the parasite is transmitted by tsetse flies to the bloodstream of mammals. Inside the mammalian host, glycolysis is essential for T. brucei and is therefore is a putative target for antitrypanosomal drugs. Other metabolic pathways may also be potential target pathways. But drugs used inside infected humans can affect a similar metabolic step in human cells. To predict which targets in metabolism may be selective we should compare the metabolic pathways in T. brucei and relevant human cells.

A genome-based metabolic map is available for both T. brucei and the human genome. For a relevant comparison, these genome-wide models should be adjusted with gene expression data to a restricted version for the bloodstream T. brucei (the clinically relevant lifecycle stage) and a liver-restricted version of the human metabolic model. These models will then be compared to elucidate differences in essentiality of metabolic genes for relevant metabolic fluxes (ATP production flux, cofactor production fluxes)