ArticleBMC genomics2009
Human liver rate-limiting enzymes influence metabolic flux via branch points and inhibitors.
Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
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- The Signaling Pathways Project, an integrated 'omics knowledgebase for mammalian cellular signaling pathways.Scientific data · 2019Article
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- Multi-tissue transcriptomics for construction of a comprehensive gene resource for the terrestrial snail Theba pisana.Scientific reports · 2016Article
- CSGene: a literature-based database for cell senescence genes and its application to identify critical cell aging pathways and associated diseases.Cell death & disease · 2016Article
- Cellular metabolic network analysis: discovering important reactions in Treponema pallidum.BioMed research international · 2015Article
- METSP: a maximum-entropy classifier based text mining tool for transporter-substrate identification with semistructured text.BioMed research international · 2015Article
- An evidence-based knowledgebase of pulmonary arterial hypertension to identify genes and pathways relevant to pathogenesis.Molecular bioSystems · 2014Article
- Human transporter database: comprehensive knowledge and discovery tools in the human transporter genes.PloS one · 2014Article
- High similarity of phylogenetic profiles of rate-limiting enzymes with inhibitory relation in Human, Mouse, Rat, budding Yeast and E. coli.BMC genomics · 2011Article
- Extending Asia Pacific bioinformatics into new realms in the "-omics" era.BMC genomics · 2009Article
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2 authors.
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Abstract
backgroundRate-limiting enzymes, because of their relatively low velocity, are believed to influence metabolic flux in pathways. To investigate their regulatory role in metabolic networks, we look at the global organization and interactions between rate-limiting enzymes and compounds such as branch point metabolites and enzyme inhibitors in human liver.
resultsBased on 96 rate-limiting enzymes and 132 branch point compounds from human liver, we found that rate-limiting enzymes surrounded 76.5% of branch points. In a compound conversion network from human liver, the 128 branch points involved showed a dramatically higher average degree, betweenness centrality and closeness centrality as a whole. Nearly half of the in vivo inhibitors were products of rate-limiting enzymes, and covered 75.34% of the inhibited targets in metabolic inhibitory networks.
conclusionFrom global topological organization, rate-limiting enzymes as a whole surround most of the branch points; so they can influence the flux through branch points. Since nearly half of the in vivo enzyme inhibitors are produced by rate-limiting enzymes in human liver, these enzymes can initiate inhibitory regulation and then influence metabolic flux through their natural products.
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