PANTHER version 10: expanded protein families and functions, and analysis tools

Mi, Huaiyu; Poudel, Sagar; Muruganujan, Anushya; Casagrande, John T.

doi:10.1093/nar/gkv1194

Cited by 793 publications

(722 citation statements)

References 20 publications

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“…Lost regions overlapping for more than 30% of their length with gaps were removed and regions within 10kb of each other were merged. Lost genes were analyzed using the PANTHER database 24 . Because PANTHER only provided adjusted p-values for fold enrichment based on binomial test, we additionally estimated the 95% confidence interval for each enriched pathways using binom.test() function in R (version 3.2.2).…”

Section: Methodsmentioning

confidence: 99%

“…Results of both EdgeR and Limma analyses are presented in Supplementary Table 2. For metabolic gene analysis, we used the list of metabolic genes obtained from the PANTHER database 24 .…”

Section: Methodsmentioning

confidence: 99%

“…To evaluate the link between the metabolic defects and specific chromosome loss, we used a statistical analysis 24 to classify the list of 1803 genes mapped to the regions lost from chromosomes 3L and 4L in t e × l s . We found that metabolic processes, particularly in glycolysis, were significantly over-represented (Extended Data Table 4).…”

mentioning

confidence: 99%

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Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus

Gibeaux

Acker

Kitaoka

et al. 2018

Nature

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Section: Methodsmentioning

confidence: 99%

“…Results of both EdgeR and Limma analyses are presented in Supplementary Table 2. For metabolic gene analysis, we used the list of metabolic genes obtained from the PANTHER database 24 .…”

Section: Methodsmentioning

confidence: 99%

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Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus

Gibeaux

Acker

Kitaoka

et al. 2018

Nature

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“…We employed the DAVID (version 6.7; RRID:SCR_001881; Huang, Sherman, & Lempicki, 2009) or PANTHER (version 10.0; RRID:SCR_004869; Mi, Poudel, Muruganujan, Casagrande, & Thomas, 2016) algorithms to analyze lists of genes with KNR or putatively novel L1 insertions for enrichment of gene ontology (GO) terms or Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. For PANTHER, only the curated “slim” GO term libraries and PANTHER pathways were queried for statistical over‐representation.…”

Section: Methodsmentioning

confidence: 99%

“…PANTHER employs a binomial distribution to calculate fold enrichment and p ‐values (Mi et al., 2016; see Appendix S1 for equations). Each algorithm adjusted the “raw” p ‐values using the Bonferroni correction for multiple testing.…”

Section: Methodsmentioning

confidence: 99%

Reading LINEs within the cocaine addicted brain

Doyle

Doucet-O’Hare²,

Hammond

et al. 2017

Brain and Behavior

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IntroductionLong interspersed element (LINE)‐1 (L1) is a type of retrotransposon capable of mobilizing into new genomic locations. Often studied in Mendelian diseases or cancer, L1s may also cause somatic mutation in the developing central nervous system. Recent reports showed L1 transcription was activated in brains of cocaine‐treated mice, and L1 retrotransposition was increased in cocaine‐treated neuronal cell cultures. We hypothesized that the predisposition to cocaine addiction may result from inherited L1s or somatic L1 mobilization in the brain.MethodsPostmortem medial prefrontal cortex (mPFC) tissue from 30 CA and 30 control individuals was studied. An Alexafluor488‐labeled NeuN antibody and fluorescence activated nuclei sorting were used to separate neuronal from non‐neuronal cell nuclei. L1s and their 3' flanking sequences were amplified from neuronal and non‐neuronal genomic DNA (gDNA) using L1‐seq. L1 DNA libraries from the neuronal gDNA were sequenced on an Illumina HiSeq2000. Sequences aligned to the hg19 human genome build were analyzed for L1 insertions using custom “L1‐seq” bioinformatics programs.ResultsPreviously uncataloged L1 insertions, some validated by PCR, were detected in neurons from both CA and control brain samples. Steady‐state L1 mRNA levels in CA and control mPFC were also assessed. Gene ontology and pathway analyses were used to assess relationships between genes putatively disrupted by novel L1s in CA and control individuals. L1 insertions in CA samples were enriched in gene ontologies and pathways previously associated with CA.ConclusionsWe conclude that neurons in the mPFC harbor L1 insertions that have the potential to influence predisposition to CA.

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Targeted O‐glycoproteomics explored increased sialylation and identified MUC16 as a poor prognosis biomarker in advanced‐stage bladder tumours

et al. 2017

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Bladder carcinogenesis and tumour progression is accompanied by profound alterations in protein glycosylation on the cell surface, which may be explored for improving disease management. In a search for prognosis biomarkers and novel therapeutic targets we have screened, using immunohistochemistry, a series of bladder tumours with differing clinicopathology for short‐chain O‐glycans commonly found in glycoproteins of human solid tumours. These included the Tn and T antigens and their sialylated counterparts sialyl‐Tn(STn) and sialyl‐T(ST), which are generally associated with poor prognosis. We have also explored the nature of T antigen sialylation, namely the sialyl‐3‐T(S3T) and sialyl‐6‐T(S6T) sialoforms, based on combinations of enzymatic treatments. We observed a predominance of sialoglycans over neutral glycoforms (Tn and T antigens) in bladder tumours. In particular, the STn antigen was associated with high‐grade disease and muscle invasion, in accordance with our previous observations. The S3T and S6T antigens were detected for the first time in bladder tumours, but not in healthy urothelia, highlighting their cancer‐specific nature. These glycans were also overexpressed in advanced lesions, especially in cases showing muscle invasion. Glycoproteomic analyses of advanced bladder tumours based on enzymatic treatments, Vicia villosa lectin‐affinity chromatography enrichment and nanoLC‐ESI‐MS/MS analysis resulted in the identification of several key cancer‐associated glycoproteins (MUC16, CD44, integrins) carrying altered glycosylation. Of particular interest were MUC16 STn+‐glycoforms, characteristic of ovarian cancers, which were found in a subset of advanced‐stage bladder tumours facing the worst prognosis. In summary, significant alterations in the O‐glycome and O‐glycoproteome of bladder tumours hold promise for the development of novel noninvasive diagnostic tools and targeted therapeutics. Furthermore, abnormal MUC16 glycoforms hold potential as surrogate biomarkers of poor prognosis and unique molecular signatures for designing highly specific targeted therapeutics.

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PANTHER version 10: expanded protein families and functions, and analysis tools

Cited by 793 publications

References 20 publications

Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus

Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus

Reading LINEs within the cocaine addicted brain

Targeted O‐glycoproteomics explored increased sialylation and identified MUC16 as a poor prognosis biomarker in advanced‐stage bladder tumours

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