Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1090880 | ENA |
REPOSITORIES: ENA
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Project description:Colorectal cancer (CRC) is the third most common cancer worldwide and liver metastasis remains the major cause of death in CRC. Extensive genomic analysis provided valuable insight into the pathogenesis and progression of CRC. However, the major proteogenomic characterization of CRC liver metastasis is still unknown. We investigated proteogenomic characterization and performed comprehensive integrative genomic analysis of human colorectal cancer liver metastasis.
2019-12-27 | GSE93286 | GEO
Project description:Zebrafish embryos are transcriptional silent until activation of the zygotic genome during the 10th cell cycle. Onset of transcription is followed by cellular and morphological changes involving cell speciation and gastrulation. Previous genome-wide surveys of transcriptional changes only assessed gene expression levels; however, recent studies have shown the necessity to map isoform-specific transcriptional changes. Here we perform isoform discovery and quantification on transcriptome sequences from before and after zebrafish zygotic genome activation (ZGA). We identify novel isoforms and isoform switches during ZGA for genes related to cell adhesion, pluripotency and DNA methylation. Isoform switching events include alternative splicing and changes in transcriptional start sites and in 3’ untranslated regions. New isoforms are identified even for well-characterized genes such as pou5f1, sall4 and dnmt1. Genes involved in cell-cell interactions such as f11r and magi1 display isoform switches with alterations of coding sequences. We also detect over 1000 transcripts that acquire a longer 3’ terminal exon when transcribed zygotically relative to the maternal transcript counterparts. ChIP-seq data mapped onto skipped exon events reveals a correlation between histone H3K36trimethylation peaks and the skipped exons, suggesting epigenetic marks being part of alternative splicing regulation. The novel isoforms and isoform switches reported here include regulators of the transcriptional, cellular and morphological changes taking place around ZGA. Our data display an array of isoform-related functional changes and represent a valuable resource complementary to existing early embryo transcriptomes. Examination H3K36me3 in zebrafish whole embryos at the Post-MBT stage
2012-11-01 | E-GEOD-40629 | biostudies-arrayexpress
Project description:Background: Histone post-translational modifications (PTMs) constitute a branch of epigenetic mechanisms that can control the expression of eukaryotic genes in a heritable manner. Recent studies have identified several PTM-binding proteins containing diverse specialized domains whose recognition of specific PTM sites leads to gene activation or repression. Here, we present a high-throughput proteogenomic platform designed to characterize the nucleosomal make-up of chromatin enriched with a set of histone PTM-binding proteins known as histone PTM readers. We support our findings with gene expression data correlating to PTM distribution. Results: We isolated human mononucleosomes bound by the bromodomain-containing proteins Brd2, Brd3 and Brd4, and by the chromodomain-containing heterochromatin proteins HP1alpha and HP1beta. Histone PTMs were quantified by mass spectrometry (ChIP-qMS), and their associated DNAs were mapped using deep sequencing. Our results reveal that Brd- and HP1-bound nucleosomes are enriched in histone PTMs consistent with actively transcribed euchromatin and silent heterochromatin, respectively. Data collected using RNA-Seq (GSM301568) show that Brd-bound sites correlate with highly expressed genes. In particular, Brd3 and Brd4 are most enriched on nucleosomes located within HOX gene clusters, whose expression is reduced upon Brd4 depletion by shRNA. Conclusions: Proteogenomic mapping of histone PTM readers, alongside the characterization of their local chromatin environments and transcriptional information, should prove useful for determining how histone PTMs are bound by these readers and how they contribute to distinct transcriptional states. Examination of Brd and HP1 proteins-binding sites in HEK293 cells.
2012-07-31 | E-GEOD-39579 | biostudies-arrayexpress
Project description:Therapeutic approaches to treat melanoma include small molecule drugs that target activating protein mutations in pro-growth signaling pathways like the MAPK pathway. While beneficial to the approximately 50% of patients with activating BRAFV600 mutation, mono- and combination therapy with MAPK inhibitors is ultimately associated with acquired resistance. To better characterize the mechanisms of MAPK inhibitor resistance in melanoma, we utilize patient-derived xenografts and apply proteogenomic approaches leveraging genomic, transcriptomic, and proteomic technologies that permit the identification of resistance-specific alterations and therapeutic vulnerabilities. A specific challenge for proteogenomic applications comes at the level of data curation to enable multi-omics data integration. Here, we present a proteogenomic approach that uses custom curated databases to identify unique resistance-specific alternations in melanoma PDX models of acquired MAPK inhibitor resistance. We demonstrate this approach with a NRASQ61L melanoma PDX model from which resistant tumors were developed following treatment with a MEK inhibitor. Our multi-omics strategy addresses current challenges in bioinformatics by leveraging development of custom curated proteogenomics databases derived from individual resistant melanoma that evolves following MEK inhibitor treatment and is scalable to comprehensively characterize acquired MAPK inhibitor resistance across patient-specific models and genomic subtypes of melanoma.
2024-05-10 | GSE266735 | GEO
Project description:We used a proteogenomic approach combining RNA-sequencing and mass spectrometry to study the MHC I-immunopeptidome specific to human iPSC samples. iPSCs were also analyzed after a 72h treatment with IFN-g (IFN-gamma) to boost MHC I levels and increase our chance for pluripotency-associated MHC I-associated peptide (paMAP) discovery. We identified 46 paMAPs which were absent from the RNA-seq of healthy somatic tissues and adult stem cells, but 40 of them were expressed in multiple cancer types from The Cancer Genome Atlas (TCGA). The antigens shared by iPSCs and tumors represent attractive targets for immunotherapy of poorly differentiated cancers.
2022-07-20 | GSE171226 | GEO
Project description:Proteogenomics is an emerging research field yet lacking a standard method of analysis. In this article, we demonstrate the strength of proteogenomic analysis specific for N-terminal data that aims at the discovery of novel translational start sites. In summary, unidentified spectra were matched to a specific N-terminal peptide library encompassing all theoretical protein N-termini encoded in the genome. Gene prediction suggested 81 protein-coding models, of which several alternative proteoforms with unannotated protein starts. Next to the proteomic data, complementary ribosome footprinting data was generated from Arabidopsis thaliana cell cultures. Translation initiation site mapping by the ribosome footprinting data provided orthogonal evidence for 14 novel peptides identified by our proteogenomics pipeline.
2016-11-25 | GSE88790 | GEO
Project description:Interventions: Case series:None
Primary outcome(s): Protein expression of each isoform of acetaldehyde dehydrogenase
Study Design: Sequential
| 2716115 | ecrin-mdr-crc