Sandbox Reserved 1056: Difference between revisions
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<StructureSection load='1F8I' size='340' side='right' caption='Isocitrate Lyase from ''Mycobacterium tuberculosis''' scene='Isocitrate Lyase complex with glyoxylate and succinate ligands bound'> | <StructureSection load='1F8I' size='340' side='right' caption='Isocitrate Lyase from ''Mycobacterium tuberculosis''' scene='Isocitrate Lyase complex with glyoxylate and succinate ligands bound'> | ||
[[Image:Glyox_Shunt.png|400 px|right|thumb|Figure 1: ICL mediated glyoxylate shunt pathway of the Citric Acid Cycle]] | [[Image:Glyox_Shunt.png|400 px|right|thumb|Figure 1: ICL mediated glyoxylate shunt pathway of the Citric Acid Cycle. The intermediates of the CAC are shown in blue, while the glyoxylate shunt pathway intermediates are shown in green.]] | ||
[http://en.wikipedia.org/wiki/Isocitrate_lyase Isocitrate Lyase] (ICL) is a metabolic enzyme that converts the metabolite isocitrate into glyoxylate and succinate. ICL is a homotetramer with each monomer being composed of 14 alpha helices, 14 beta sheets, and a magnesium ion cofactor. ICL has shown clinical relevance in the disease state [http://en.wikipedia.org/wiki/Tuberculosis Tuberculosis] where it is responsible for the persistence of ''Mycobacterium tuberculosis'' during the chronic stage of infection<ref name="genes">PMID: 18054522</ref> This survival strategy mediated by ICL is characterized by a metabolic shortcut within the [http://en.wikipedia.org/wiki/Citric_acid_cycle Citric Acid Cycle]. ICL creates this shunt pathway by converting isocitrate to succinate and glyoxylate, diverting acetyl-CoA from the beta-oxidation of fatty acids<ref name="ICL">PMID:10932251</ref><ref name="ICL2">PMID: 2696959</ref>. | [http://en.wikipedia.org/wiki/Isocitrate_lyase Isocitrate Lyase] (ICL) is a metabolic enzyme that converts the metabolite isocitrate into glyoxylate and succinate. ICL is a homotetramer with each monomer being composed of 14 alpha helices, 14 beta sheets, and a magnesium ion cofactor. ICL has shown clinical relevance in the disease state [http://en.wikipedia.org/wiki/Tuberculosis Tuberculosis] where it is responsible for the persistence of ''Mycobacterium tuberculosis'' during the chronic stage of infection<ref name="genes">PMID: 18054522</ref> This survival strategy mediated by ICL is characterized by a metabolic shortcut within the [http://en.wikipedia.org/wiki/Citric_acid_cycle Citric Acid Cycle]. ICL creates this shunt pathway by converting isocitrate to succinate and glyoxylate, diverting acetyl-CoA from the beta-oxidation of fatty acids<ref name="ICL">PMID:10932251</ref><ref name="ICL2">PMID: 2696959</ref>. | ||