Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Plasma Proteome for Hepatobiliary Carcinomas

ABSTRACT: This project is to identify plasma glycoprotein markers for hepatobiliary cancers

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Plasma

DISEASE(S): Cholangiocarcinoma

SUBMITTER: ChengHsun Ho

LAB HEAD: ChengHsun Ho

PROVIDER: PXD013629 | Pride | 2019-11-12

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	CCA01.csv	Csv
	CCA01.mgf	Mgf
	CCA01.mzXML	Mzxml
	CCA02.csv	Csv
	CCA02.mgf	Mgf

Items per page:

1 - 5 of 945

Publications

Plasma proteome plus site-specific N-glycoprofiling for hepatobiliary carcinomas.

Chang Ting-Tsung TT Cheng Ji-Hong JH Tsai Hung-Wen HW Young Kung-Chia KC Hsieh Sun-Yuan SY Ho Cheng-Hsun CH

The journal of pathology. Clinical research 20190625 3

Hepatobiliary cancer is the third leading cause of cancer death worldwide. Appropriate markers for early diagnosis, monitoring of disease progression, and prediction of postsurgical outcome are still lacking. As the majority of circulating N-glycoproteins are originated from the hepatobiliary system, we sought to explore new markers by assessing the dynamics of N-glycoproteome in plasma samples from patients with hepatocellular carcinoma (HCC), cholangiocarcinoma (CCA), or combined HCC and CCA ( ...[more]

PMID: 31136099

Similar Datasets

Huntingtin inclusions trigger cellular quiescence, deactivate apoptosis and lead to delayed necrosis

Project description:Two popular models for how mutant Huntingtin exon 1 (Httex1) aggregation into inclusions relates to pathogenesis involve seemingly contradictory mechanisms. In one model, inclusions are adaptive by sequestering the proteotoxicity of soluble Httex1. In the other, inclusions compromise cellular activity from proteome co-aggregation. Via a biosensor of Httex1 conformation in mammalian cell models, we discovered a mechanism that explains this contradiction. Newly-formed inclusions are comprised of disordered Httex1 and ribonucleoproteins. As inclusions matured, Httex1 reconfigured into amyloid, and other glutamine-rich and prion-domain containing proteins were recruited. Soluble Httex1 caused a hyperpolarized mitochondrial membrane potential, increased reactive oxygen species and promoted apoptosis. Inclusion formation triggered a collapsed mitochondrial potential, cellular quiescence, and deactivated apoptosis. We propose a revised model where both soluble Httex1 and inclusions are toxic, yet inclusions impair programmed cell death arising from stalled cellular functioning. Hence cells live longer in a metabolically quiescent state and ultimately die by necrosis.

2017-05-04 | PXD005120 | Pride

A primate nigrostriatal atlas of neuronal vulnerability and resilience in a model of Parkinson’s disease

Project description:The degenerative process in Parkinson’s disease (PD) causes a progressive loss of dopaminergic neurons (DaNs) in the nigrostriatal system. Resolving the differences in neuronal susceptibility warrants an amenable PD model that, in comparison to post-mortem human specimens, controls for environmental and genetic differences in PD pathogenesis. At present study, we generated a primate model of PD by carotid artery injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine MPTP and sampled substantia nigra and putamen of macaque for single cell sequencing analysis.

2023-11-19 | E-MTAB-13437 | biostudies-arrayexpress

mRNA Expression data from rats treated with ANIT or vehicle

Project description:Adult Sprague Dawley rats were treated i.g. with 50 mg/kg alpha-naphthylisothiocyanate (ANIT) or vehicle (corn oil). Hepatobiliary liver injury occurred at 24 h postdose in ANIT rats with repair at 120h. Livers were extracted from rats at 24h and 120 h post ANIT exposure. This study investigated differences in mRNA expression between the injury and repair phases in the context of ANIT exposure. 8 week male Sprague Dawley rats were administered ANIT or vehicle for quantification of hepatobiliary injury via clinical chemistry biomarkers and pathology between 6 and 168 h postdosing. Rats sacrificed at 24 h and 120h postdosing coincided with peak injury and injury resolution, respectively.

2015-08-26 | E-GEOD-72387 | biostudies-arrayexpress

RNAseq of ZC3H5 interacting mRNA

Project description:Bloodstream-form trypanosomes (Lister 427) constitutively expressing ZC3H5-TAP (Tb927.3.740) were used. The protein was pulled down with an IgG column , then the protein and bound RNA was eluted using TEV protease. RNA was then sequenced from unbound (flow-through) and bound (eluate) fractions.

2020-06-06 | E-MTAB-9084 | biostudies-arrayexpress

Role for HA and the viral RNA polymerase complex in the virulence of the 1918 influenza virus

Project description:The goal of this experiment was to examine the biological properties of reassortant viruses between the 1918 virus and a contemporary human H1N1 virus to determine the role of hemagglutinin (HA) and the viral RNA polymerase complex of 1918 virus toward pathogenesis and abberant host responses in mice. Six- to eight-week-old female BALB/c mice were anesthetized and inoculated with 50 μl of phosphate-buffered saline (PBS; Mock) or with 10^6 pfu of virus in a 50 μl volume. There are a total of six biological conditions: wild-type 1918 virus (A/Brevig Mission/1/1918; 1918), wild-type K173 virus (A/Kawasaki/173/2001; K173), three reassortant viruses between 1918 and K173 viruses [1918HA/K173, 1918PB1/K173, and 1918(3P+NP)/K173], and mock-infected control animals. Nine animals per virus group were inoculated, and whole lungs were collected at 1, 3 and 5 days post-inoculation from three animals per virus group per time point. Two of three mice inoculated with 1918 virus and 1918HA/K173 virus died by day 5 post-inoculation. Six animals were inoculated with PBS. Whole lungs from two mock-infected animals per time point were collected and served as the uninfected reference. All samples were processed for lung gene expression analysis using oligonucleotide microarrays. Technical replicates were performed for 9 samples.

2013-02-23 | E-GEOD-44595 | biostudies-arrayexpress

Plasmodium ARK2 and EB1 drives the unconventional spindle dynamics, during chromosome segregation in sexual transmission stages

Project description:The Aurora family of kinases orchestrates chromosome segregation and cytokinesis during cell division, with precise spatiotemporal regulation of its catalytic activities by distinct protein scaffolds. Plasmodium spp., the causative agents of malaria, are unicellular eukaryotes with three unique and highly divergent aurora-related kinases (ARK1-3) that are essential for asexual cellular proliferation, but lack most canonical scaffolds/activators. Here we investigate the role of ARK2 during sexual proliferation of the rodent malaria Plasmodium berghei, using a combination of super-resolution microscopy, mass spectrometry, and live-cell fluorescence imaging. We find that ARK2 is primarily located at spindle apparatus microtubules in the vicinity of kinetochores during both mitosis and meiosis. Interactomic and co-localisation studies reveal several putative ARK2-associated interactors including the microtubule plus end-binding protein EB1, together with MISFIT and Myosin-K, but no conserved eukaryotic scaffold proteins. Gene function studies indicate that ARK2 and EB1 are complementary in driving endomitotic division and thereby parasite transmission through the mosquito. This discovery underlines the flexibility of molecular networks to rewire and drive unconventional mechanisms of chromosome segregation in the malaria parasite.

2023-08-15 | PXD043164 | Pride

Role of the Ccr4/Not complex in the regulation of heterochromatin in Schizosaccharomyces pombe

Project description:ChIP-seq experiments to investigate heterochromatin structure in wild type, caf1, ccr4 and mmi1 mutants of fission yeast

2015-09-28 | E-MTAB-3036 | biostudies-arrayexpress

Role of the Ccr4/Not complex in the regulation of heterochromatin in Schizosaccharomyces pombe (VIII)

Project description:Distribution of Chp1 protein on S. pombe chromosomes analysed by CHIP-seq in wild type cells and ccr4 mutants

2015-09-28 | E-MTAB-3705 | biostudies-arrayexpress

A single N66S mutation in the PB1-F2 protein of influenza A virus increases virulence by inhibiting the early interferon response in vivo

Project description:This study used virological, histological, and global gene expression from an experimental murine model of influenza infection to study the contribution of a specific mutation in the PB1-F2 protein (PB1-F2 N66S) of influenza A to viral pathogenesis. 6-8 week old, wild-type, female, C57Bl/6 mice were inoculated individually with 30 μl (10^4 PFU) of virus (recombinant influenza A/WSN/33 carrying the PB1 gene segment from A/Hong Kong/156/97 (H5N1) or a PB1 mutant recombinant virus resulting in an amino acid change at position 66 in the PB1-F2 protein [N66S]) in phosphate-buffered saline (PBS) containing penicillin-streptomycin and bovine serum albumin (PBS-BA-PS). A total of 10^4 PFU of virus was given in all inoculations. Control mice were given PBS-BA-PS. Lung samples were taken for microarray analysis at 12h, 1d, 3d, and 5d post-infection (n=3 animals per group at each time point for virus infected animals; n=2 animals per time point for mock-infected animals).

2012-02-20 | E-GEOD-35940 | biostudies-arrayexpress

Transcription profiling of mouse quantitative trait loci (QTLs) in uantitative trait loci (QTLs) and brain to identify genes and loci that control hematopoietic stem cell (HSC) functioning

Project description:We have combined large-scale mRNA expression and gene mapping methods to identify genes and loci that control hematopoietic stem cell (HSC) functioning. mRNA expression levels were measured in purified HSC isolated from a panel of densely genotyped recombinant inbred mouse strains. Quantitative trait loci (QTLs) associated with variation in expression of thousands of transcripts were mapped. Comparison of the physical transcript position with the location of the controlling QTL identified polymorphic cis-acting stem cell genes. In addition, multiple trans-acting control loci were highlighted that modify expression of large numbers of genes. These groups of co-regulated transcripts identify pathways that specify variation in stem cells. We illustrate this concept with the identification of strong candidate genes involved with HSC turnover. We compared expression QTLs in HSC and brain from the same animals, and document both shared and tissue-specific QTLs. Our data are accessible through WebQTL, a web-based interface that allows custom genetic linkage analysis and identification of co-regulated transcripts.

2007-11-16 | E-GEOD-2031 | biostudies-arrayexpress