Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteome-wide identification of arginine methylation in colorectal cancer tissues from patients

ABSTRACT: High-throughput identification of arginine methylation using clinical samples has not previously been studied.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Colon

DISEASE(S): Colon Cancer

SUBMITTER: Ju Yeon Lee

LAB HEAD: Hee Cheol Kim

PROVIDER: PXD011765 | Pride | 2020-08-05

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

Proteome-wide identification of arginine methylation in colorectal cancer tissues from patients.

Lim Yongchul Y Lee Ju Yeon JY Ha Su Jin SJ Yu Suyeun S Shin Jung Kyong JK Kim Hee Cheol HC

Proteome science 20200519

<h4>Background</h4>Protein arginine methylation reaction is catalyzed by protein arginine methyltransferase (PRMT) and the modification is implicated in various diseases including cancer. Currently, thousands of arginine methylation sites have been identified using high-resolution mass spectrometry-based proteomics technology. However, identification of arginine methylation using clinical samples at proteome level has not been reported yet. The objective of the present study was to identify, mon ...[more]

PMID: 32467672

Similar Datasets

IFITM3 amino acid mutants phosphoproteomics

Project description:To investigate the role of IFITM3 in B-ALL, patient derived xenograft cells PDX2 were transduced with either a the constitutively membrane associated IFITM3-Y20E mutant or EV control. Additional mutation of PIP3 binding sites within the conserved internal loop region - K83/K104 or R85/R87/K88 - were introduced to test the predicted function of these sites.

2020-12-18 | PXD020696 | Pride

PRMT5 methyl proteomics in MiaPaca2 cells

Project description:Goal: To determine total PRMT5 methyl substrates and those that function through the novel substrate adaptor binding site

2022-06-13 | PXD019991 | Pride

Targeting HDAC6 to treat heart failure with preserved ejection fraction, Mouse heart LC-MS with PTMscan

Project description:Heart failure with preserved ejection fraction (HFpEF) poses therapeutic challenges due to the limited treatment options. Building upon our previous research that demonstrates the efficacy of histone deacetylase 6 (HDAC6) inhibition in a genetic cardiomyopathy model, we investigate HDAC6’s role in HFpEF due to their shared mechanisms of inflammation and metabolism. Here, we show that inhibiting HDAC6 with TYA-018 effectively reverses established heart failure and its associated symptoms in HFpEF mouse models. Additionally, in mice lacking the Hdac6 gene, HFpEF progression is delayed and they are resistant to TYA-018’s effects. The efficacy of TYA-018 is comparable to a sodium-glucose cotransporter 2 (SGLT2) inhibitor, and their combination shows enhanced effects. Mechanistically, TYA-018 restores gene expression related to hypertrophy, fibrosis, and mitochondrial energy production in HFpEF heart tissues. Furthermore, TYA-018 also inhibits activation of human cardiac fibroblasts and enhances mitochondrial respiratory capacity in cardiomyocytes. In this work, our findings show that HDAC6 impacts heart pathophysiology and is a promising target for HFpEF treatment.

2024-01-17 | PXD048363 | Pride

S6K1 Phosphoproteome in Tsc1-null mouse kidney iMCD3 cells

Project description:Loss of Tsc1 in the kidneys gives rise to rapid polycystogenesis and kidney failure due to the hyperactivation of mTOR complex I (mTORC1). One of the major downstream targets of mTORC1 is S6K1, which is responsible for driving many of the effector functions of mTOR. Strikingly, the loss of S6k1 in the context of hyperactivated mTOR is sufficient to reverse the generation of polycystic kidneys. In an effort to uncover novel direct S6k1 substrates involved in the generation of cystic kidneys, we generated Tsc1-null and Tsc1/S6k1-double null murine inner medullary collecting duct (iMCD3) cell lines using CRISPR/Cas9. Using these two cell lines, we conducted a phosphoproteome screen to search for novel candidates. Using a combination of antibody-motif enrichment and metal affinity enrichment, we provide a comprehensive phosphoproteome profile between these two genotypes.

2020-08-11 | PXD014832 | Pride

Comprehensive analysis of symmetric arginine dimethylation in colorectal cancer tissues from patients using immuniaffinity enrichment followed by LC-MS/MS analysis

Project description:Post-translational arginine methylation is responsible for regulation of a variety of biological processes. The protein arginine methyltransferase 5 (PRMT5) is the major enzyme responsible for generating monomethyl- and symmetric dimethyl arginine (MMA and SDMA, respectively) in proteins. PRMT5 is essential for viability and normal development, and overexpressed in a wide variety of cancer types. In the present study, we found that the levels of PRMT5 and symmetric dimethylation in proteins from colorectal cancer (CRC) tissues are more highly maintained relative to adjacent normal tissues from patients. Using immunoaffinity enrichment of methylated peptides combined with high resolution mass spectrometry, a total of 147 SDMA sites from 94 proteins were identified. Most abundant methylated proteins identified from normal and CRC tissues are RNA processing proteins, transcriptional and translational regulators. Furthermore, when quantitative analysis of the two tissue types of samples was carried out, 77 SDMA sites exhibited statistically significant changes (>2.0-fold, p-value <0.05) between normal and CRC tissues. We confirmed KSRP, G3BP2 and TRIP6 which are more highly maintained in cancer tissues relative to adjacent normal tissues from same patients as well as the expression levels of the proteins. This study is the first comprehensive analysis of symmetric arginine dimethylation using clinical samples and suggests that the modification can be used in clinical application.

2020-06-01 | PXD015653 | Pride

Dynamic changes of DNA methylome and hydroxymethylome during neural differentiation of hES cell (hMeDIP-Seq and MBD-Seq)

Project description:DNA methylation and hydroxymethylation have been implicated in normal development and differentiation, but our knowledge about the genome-wide distribution of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) during cellular differentiation remains limited. Using in vitro model system of gradual differentiation of human embryonic stem (hES) cells into ventral midbrain-type neural precursor (NP) cells and terminally into dopamine (DA) neurons, we explored changes in 5mC or 5hmC patterns during lineage commitment. We used three techniques, 450K DNA methylation array, MBD-seq, and hMeDIP-seq, and found combination of these methods can provide comprehensive information on the genome-wide 5mC or 5hmC patterns. We observed dramatic changes of 5mC patterns during differentiation of hES cells into NP cells. Although genome-wide 5hmC distribution was more stable than 5mC, coding exons, CpG islands and shores showed dynamic 5hmC patterns during differentiation. In addition to the role of DNA methylation as a mechanism to initiating gene silencing, we also found DNA methylation as a locking system to maintain gene silencing. More than 1,000 genes including mesoderm development related genes acquired promoter methylation during neuronal differentiation even though they were already silenced in hES cells. Finally, we found that activated genes lost 5mC in transcription start site (TSS) but acquired 5hmC around TSS and gene body during differentiation. Our findings may provide clues for elucidating the molecular mechanisms underlying lineage specific differentiation of pluripotent stem cells during human embryonic development. Examination of hMeDIP-Seq and MBD-Seq in 3 cell types (human embryonic stem, neural precursor, and dopamine neuron cells)

2013-11-04 | E-GEOD-38214 | biostudies-arrayexpress

Dynamic changes of DNA methylome and hydroxymethylome during neural differentiation of hES cells (Methylation BeadChip)

Project description:DNA methylation and hydroxymethylation have been implicated in normal development and differentiation, but our knowledge about the genome-wide distribution of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) during cellular differentiation remains limited. Using in vitro model system of gradual differentiation of human embryonic stem (hES) cells into ventral midbrain-type neural precursor (NP) cells and terminally into dopamine (DA) neurons, we explored changes in 5mC or 5hmC patterns during lineage commitment. We used three techniques, 450K DNA methylation array, MBD-seq, and hMeDIP-seq, and found combination of these methods can provide comprehensive information on the genome-wide 5mC or 5hmC patterns. We observed dramatic changes of 5mC patterns during differentiation of hES cells into NP cells. Although genome-wide 5hmC distribution was more stable than 5mC, coding exons, CpG islands and shores showed dynamic 5hmC patterns during differentiation. In addition to the role of DNA methylation as a mechanism to initiating gene silencing, we also found DNA methylation as a locking system to maintain gene silencing. More than 1,000 genes including mesoderm development related genes acquired promoter methylation during neuronal differentiation even though they were already silenced in hES cells. Finally, we found that activated genes lost 5mC in transcription start site (TSS) but acquired 5hmC around TSS and gene body during differentiation. Our findings may provide clues for elucidating the molecular mechanisms underlying lineage specific differentiation of pluripotent stem cells during human embryonic development. Examination of genome-wide DNA methylation in 3 cell types (human embryonic stem, neural precursor, and dopamine neuron cells)

2013-11-04 | E-GEOD-38216 | biostudies-arrayexpress

Arginine (di)methylated Human Leukocyte Antigen class I peptides are favorably presented by HLA-B*07

Project description:Specific alterations in protein post-translational modification (PTMs) are recognized hallmarks of diseases. These modifications potentially provide a unique disease-related source of Human Leukocyte Antigen (HLA) class I-presented peptide antigens that can elicit specific immune responses. Although, phosphorylated HLA peptides have received already some attention, the frequency and characteristics of arginine methylated HLA class I peptide presentation have not been explored in detail. In a model human B-cell line we detected by mass spectrometry (MS) 149 HLA class I peptides harboring mono- and/or di-methylated arginine residues. The source proteins of these antigens play important roles in signal transduction, gene transcription and DNA repair. A striking preference was observed in presentation of arginine (di)methylated peptides predicted to bind HLA-B*07 molecules, most likely because the binding motifs of this allele resemble the substrates for arginine methyl-transferases. The HLA-B*07 peptides were preferentially di-methylated at the P3 position in the sequence, thus consecutively to the proline anchor residue at position P2. Such a proline-arginine sequnce has been associated with the arginine methyl-transferases CARM1 and PRMT5. Making use of the specific neutral losses in the MS/MS spectra we could further assign most of the peptides to be asymmetrically di-methylated, most likely by CARM1. The here presented data expand our knowledge of processing and presentation of arginine (di)methylated HLA class I peptides, indicating that this type of modification is frequently presented for recognition by T-cells and might thus present a potential target for immunotherapy.

2016-08-15 | PXD004233 | Pride

Promoter methylation data from genomic DNA in patient with rectal cancer

Project description:The identification of surrogate methylation markers that can predict responses to preoperative chemoradiotherapy (CRT) in rectal cancer patients. Genome-wide association studies in clinical populations are theoretically capable of identifying markers that are capable of tumor regression after CRT. We used InfiniumM-BM-. Methylation Assay to detail methylation status of patientM-bM-^@M-^Ys group showing differential responsiveness to preoperative CRT and profiled SNP biomarkers. The chemoradiosensitivity of tumor tissue from the initial cohort of 45 patients was assessed using clinical responses of tumor regression grade (TRG). TRG was clinically categorized as complete response (CR) as TRG 1, dominant response (ER or finally as DR) as TRG 1 and 2, and efficient response (RYN or finally as ER) as TRG 1, 2, and 3 (TRG grade from Mandard et al, 1994). Examination of genome-wide DNA methylation in 45 colon cancer tissues. We separated patients into TRG1,2,3,4 and 5 group after chemoradiotherapy(CRT). As proposed by Mandard et al. TRG 1, complete tumor response; TRG2, residual cancer cells scattered through fibrosis; TRG 3, an increased number of residual cancer cells, with predominant fibrosis; TRG 4, residual cancer outgrowing fibrosis; and TRG 5, no regressive changes within the tumor: Responders (TRG 1 and 2) and nonresponders (TRG 3?5). Mandard et al. Cancer 1994 Group 1 and Group 2 in ER, CR and RYN was divided by TRG classification. CR: group 1 - TRG 2,3,4 and 5; group 2 - TRG 1 ER: group 1 - TRG 3,4,5; group 2 - TRG 1 and 2 RYN: group 1 - TRG 4 and 5; group 2 - TRG 1,2 and 3

2014-08-01 | E-GEOD-39958 | biostudies-arrayexpress

Genome-wide profiling and validation for forensic tissue-specific DNA methylation markers

Project description:Forensic body fluid identification is important for crime scene reconstruction. We used Illumina HumanMethylation 450K bead array containing over the 450,000 CpG sites in 16 body fluid samples to find novel DNA methylation marker for forensic body fluid identification. Examination of genome-wide DNA methylation profiling in 16 body fluid samples

2014-07-31 | E-GEOD-55734 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data