PathPred: an enzyme-catalyzed metabolic pathway prediction server

Abstract

The KEGG RPAIR database is a collection of biochemical structure transformation patterns, called RDM patterns, and chemical structure alignments of substrate-product pairs (reactant pairs) in all known enzyme-catalyzed reactions taken from the Enzyme Nomenclature and the KEGG PATHWAY database. Here, we present PathPred (http://www.genome.jp/tools/pathpred/), a web-based server to predict plausible pathways of muti-step reactions starting from a query compound, based on the local RDM pattern match and the global chemical structure alignment against the reactant pair library. In this server, we focus on predicting pathways for microbial biodegradation of environmental compounds and biosynthesis of plant secondary metabolites, which correspond to characteristic RDM patterns in 947 and 1397 reactant pairs, respectively. The server provides transformed compounds and reference transformation patterns in each predicted reaction, and displays all predicted multi-step reaction pathways in a tree-shaped graph.

Applications of genome-scale metabolic network model in metabolic engineering

“…OptStrain [67], OptReg [68], OptForce [72], k-OptForce [16], OptORF [44], CosMos [20] Omics data integration Transcriptome GIMME [5], iMAT [82], GIM 3 E [76], E-Flux [18], PROM [13], MADE [38], tFBA [90], RELATCH [45], TEAM [19], AdaM [89], GX-FBA [60], mCADRE [92], FCGs [43], EXAMO [75], TIGER [37] Proteome GIMMEp [6] Pathway prediction BNICE [29], Cho et al [14], RetroPath [11], PathPred [59], DESHARKY [74], BioPath [94], XTMS [12], GEM-Path [56] phenotype and gene essentiality [24]. Even further, taking advantage of a large set of genome sequences available for various E. coli strains, the GEMs for 55 E. coli strains were used to investigate the variations in gene, reaction and metabolite contents, and the capabilities to adapt to different nutritional environments among the strains [40].…”

“…BNICE also takes into account reaction thermodynamics and the entries in BNICE are not limited to the chemicals from a specific database such as KEGG LIGAND facilitating the prediction of novel synthetic pathways. Various prediction algorithms, including the pathway prediction system developed by Cho et al [14], RetroPath [11], PathPred [59], DESHARKY [74] and Biopathway Predictor (BioPath), have been developed using their own reaction rules and the heuristics for ranking and pathway search algorithms (Table 1) [94].…”

New developments in the trace analysis of organic water pollutants

“…The occurrence of human metabolites and the formation of microbial transformation products of seven pharmaceuticals and of one biocide, predicted by various computed-based biotransformation pathway prediction systems like UM-PPS (Ellis et al 2006), CATABOL (Dimitrov et al 2007, and PathPred (Moriya et al 2010), were targeted by HPLC-high-resolution-MS/MS in activated sludge-seeded batch reactors (Kern et al 2010). Except one, all of the 12 TPs identified could also be detected in the effluents of two full-scale municipal WWTPs.…”

Mitochondrial Free Radicals, Antioxidants, Nutrient Substances, and Chronic Hepatitis C

“…HCV-induced ROS generation suppresses the expression of hepcidin (i.e., a peptide which regulate Fe metabolism by decreasing Fe absorption), facilitating the Fe overload; whereas hepcidin expression was restored by antioxidants (Miura et al, 2008). Fe overload in vitro were observed to cause further ROS augmentation and amplify the expression of catalase, Cu,Zn-SOD, and NADPH dehydrogenase (Moriya et al, 2010). These observations presented that increased intracellular Fe and oxidative stress, in turn, aggravates HCV-induced mitochondrial damage.…”

“…HCV core proteins induced ROS generation leads to a decreased hepcidin expression also contribute to Fe accumulation (Nagashima et al, 2006). Fe overload induced hepatic 8-oxo-dG and eventually increased mitochondrial injury and the risk of hepatocellular carcinoma development Moriya et al, 2010). Thus, increased oxidative stress and altered mitochondrial function both in vitro and in vivo is proven to be involved in chronic hepatitis C infection and is thought to contribute to its progression.…”