KOBAS 2.0: a web server for annotation and identification of enriched pathways and diseases

Xie, Chen; Mao, Xizeng; Huang, Jiaju; Ding, Yang; Wu, Jianmin; Dong, Shan; Kong, Lei; Gao, Ge; Li, Chuan Yun; Wei, Liping

doi:10.1093/nar/gkr483

Cited by 4,093 publications

(2,805 citation statements)

References 43 publications

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“…Probes also were assigned to maize KEGG genes and KEGG pathway terms using Kobas 2.0 (mapping e , 0.01; Xie et al, 2011). A hypergeometric distribution test with Yekutieli correction also was applied to identify overrepresented KEGG pathways.…”

Section: Annotation Of Microarray Results and Analysis Of Go Terms Anmentioning

confidence: 99%

“…Differentially expressed probes were assigned Gene Ontology (GO) terms using the AgriGO platform (Du et al, 2010) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways using Kobas 2.0 (Xie et al, 2011). We assessed whether certain GO terms or KEGG pathways might be significantly enriched in our data sets (Table I).…”

Section: Genome-wide Transcriptional Response Of Maize Seedlings To Wtsementioning

confidence: 99%

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Perturbation of Maize Phenylpropanoid Metabolism by an AvrE Family Type III Effector fromPantoea stewartii

et al. 2015

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Republic of Korea (S.-M.P., M.G.K.)AvrE family type III effector proteins share the ability to suppress host defenses, induce disease-associated cell death, and promote bacterial growth. However, despite widespread contributions to numerous bacterial diseases in agriculturally important plants, the mode of action of these effectors remains largely unknown. WtsE is an AvrE family member required for the ability of Pantoea stewartii ssp. stewartii (Pnss) to proliferate efficiently and cause wilt and leaf blight symptoms in maize (Zea mays) plants. Notably, when WtsE is delivered by a heterologous system into the leaf cells of susceptible maize seedlings, it alone produces water-soaked disease symptoms reminiscent of those produced by Pnss. Thus, WtsE is a pathogenicity and virulence factor in maize, and an Escherichia coli heterologous delivery system can be used to study the activity of WtsE in isolation from other factors produced by Pnss. Transcriptional profiling of maize revealed the effects of WtsE, including induction of genes involved in secondary metabolism and suppression of genes involved in photosynthesis. Targeted metabolite quantification revealed that WtsE perturbs maize metabolism, including the induction of coumaroyl tyramine. The ability of mutant WtsE derivatives to elicit transcriptional and metabolic changes in susceptible maize seedlings correlated with their ability to promote disease. Furthermore, chemical inhibitors that block metabolic flux into the phenylpropanoid pathways targeted by WtsE also disrupted the pathogenicity and virulence activity of WtsE. While numerous metabolites produced downstream of the shikimate pathway are known to promote plant defense, our results indicate that misregulated induction of phenylpropanoid metabolism also can be used to promote pathogen virulence.

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Section: Annotation Of Microarray Results and Analysis Of Go Terms Anmentioning

confidence: 99%

Section: Genome-wide Transcriptional Response Of Maize Seedlings To Wtsementioning

confidence: 99%

Perturbation of Maize Phenylpropanoid Metabolism by an AvrE Family Type III Effector fromPantoea stewartii

et al. 2015

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“…Multiple alignment reads were discarded. The RPKM scores for each gene were calculated as previously described [55]. A series of Perl (v5.12.2) and R (v2.13.1) scripts were implemented to evaluate the quality of the RNA-seq experiments.…”

Section: Rna-seq and Microarray Data Analysis And Miningmentioning

confidence: 99%

Hydrogen peroxide primes heart regeneration with a derepression mechanism

et al. 2014

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While the adult human heart has very limited regenerative potential, the adult zebrafish heart can fully regenerate after 20% ventricular resection. Although previous reports suggest that developmental signaling pathways such as FGF and PDGF are reused in adult heart regeneration, the underlying intracellular mechanisms remain largely unknown. Here we show that H 2 O 2 acts as a novel epicardial and myocardial signal to prime the heart for regeneration in adult zebrafish. Live imaging of intact hearts revealed highly localized H 2 O 2 (~30 µM) production in the epicardium and adjacent compact myocardium at the resection site. Decreasing H 2 O 2 formation with the Duox inhibitors diphenyleneiodonium (DPI) or apocynin, or scavenging H 2 O 2 by catalase overexpression markedly impaired cardiac regeneration while exogenous H 2 O 2 rescued the inhibitory effects of DPI on cardiac regeneration, indicating that H 2 O 2 is an essential and sufficient signal in this process. Mechanistically, elevated H 2 O 2 destabilized the redox-sensitive phosphatase Dusp6 and hence increased the phosphorylation of Erk1/2. The Dusp6 inhibitor BCI achieved similar pro-regenerative effects while transgenic overexpression of dusp6 impaired cardiac regeneration. H 2 O 2 plays a dual role in recruiting immune cells and promoting heart regeneration through two relatively independent pathways. We conclude that H 2 O 2 potentially generated from Duox/Nox2 promotes heart regeneration in zebrafish by unleashing MAP kinase signaling through a derepression mechanism involving Dusp6.

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“…KOBAS was used to perform pathway enrichment analysis (21). The hypergeometric test was selected to test statistical enrichment of KEGG and Reactome pathways, and the P values were corrected for multiple comparisons (22).…”

Section: Pathway Enrichment and Protein-protein Interaction Network Amentioning

confidence: 99%

Phosphoproteomic Profiling Identifies Focal Adhesion Kinase as a Mediator of Docetaxel Resistance in Castrate-Resistant Prostate Cancer

Lee

Hochgräfe

Lin

et al. 2014

Molecular Cancer Therapeutics

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Docetaxel remains the standard-of-care for men diagnosed with metastatic castrate-resistant prostate cancer (CRPC). However, only approximately 50% of patients benefit from treatment and all develop docetaxelresistant disease. Here, we characterize global perturbations in tyrosine kinase signaling associated with docetaxel resistance and thereby develop a potential therapeutic strategy to reverse this phenotype. Using quantitative mass spectrometry-based phosphoproteomics, we identified that metastatic docetaxel-resistant prostate cancer cell lines (DU145-Rx and PC3-Rx) exhibit increased phosphorylation of focal adhesion kinase (FAK) on Y397 and Y576, in comparison with parental controls (DU145 and PC3, respectively). Bioinformatic analyses identified perturbations in pathways regulating focal adhesions and the actin cytoskeleton and in protein-protein interaction networks related to these pathways in docetaxel-resistant cells. Treatment with the FAK tyrosine kinase inhibitor (TKI) PF-00562271 reduced FAK phosphorylation in the resistant cells, but did not affect cell viability or Akt phosphorylation. Docetaxel administration reduced FAK and Akt phosphorylation, whereas cotreatment with PF-00562271 and docetaxel resulted in an additive attenuation of FAK and Akt phosphorylation and overcame the chemoresistant phenotype. The enhanced efficacy of cotreatment was due to increased autophagic cell death, rather than apoptosis. These data strongly support that enhanced FAK activation mediates chemoresistance in CRPC, and identify a potential clinical niche for FAK TKIs, where coadministration with docetaxel may be used in patients with CRPC to overcome chemoresistance. Mol Cancer Ther; 13(1); 190-201. Ó2013 AACR.

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KOBAS 2.0: a web server for annotation and identification of enriched pathways and diseases

Cited by 4,093 publications

References 43 publications

Perturbation of Maize Phenylpropanoid Metabolism by an AvrE Family Type III Effector fromPantoea stewartii

Perturbation of Maize Phenylpropanoid Metabolism by an AvrE Family Type III Effector fromPantoea stewartii

Hydrogen peroxide primes heart regeneration with a derepression mechanism

Phosphoproteomic Profiling Identifies Focal Adhesion Kinase as a Mediator of Docetaxel Resistance in Castrate-Resistant Prostate Cancer

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