Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

364ac256-2092-4b42-bb6c-c36cd70e79aa - samples

ABSTRACT: RNAseq data from Passman et al 2023. Clonal CCO-deficient hepatocyte patches and nearby CCO-proficient hepatocytes were identified in morphologically normal human livers and sampled at varying distances along the PT-CV axis. Samples are characterised according to their location within the liver lobule, with "PT" denoting samples abutting the portal triad, "CV" denoting samples abutting the central hepatic vein, and "Mid" sampled acquired midway between these structures. Analysis was performed on an Illumina Nextseq using a high output kit and 100 single-end cycles.

PROVIDER: EGAD00001010033 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Clonal dynamics of normal hepatocyte expansions in homeostatic human livers and their association with the biliary epithelium

Project description:BAM files containing paired-end mtDNA sequencing data from morphologically normal human liver. CCO-proficient hepatocytes acquired from livers in which clonal CCO-deficient hepatocyte patches had been previously identified. Individual BAM files are named according to their patch, line and sample location, where PT denotes tissue near to the portal triad (PT), central hepatic vein (CV) and midway between these two structures (Mid). "Stroma" control samples were used for identifying germ-line variants. Sequenced on NextSeq 500 platform.

| EGAS00001006962 | EGA

0bf3ef30-d3f9-47cb-8c57-75d5c62c7306 - samples

Project description:BAM files containing paired-end mtDNA sequencing data from morphologically normal human liver. CCO-proficient hepatocytes acquired from human livers in which clonal CCO-deficient hepatocyte patches had been previously identified. Individual BAM files are named according to their patch, line and sample location, where PT denotes tissue near to the portal triad (PT), central hepatic vein (CV) and midway between these two structures (Mid). "Stroma" control samples were used for identifying germ-line variants. Sequenced on NextSeq 500 platform.

| EGAD00001010016 | EGA

RNA sequencing of CCO- and CCO+ human hepatocytes

Project description:RNAseq data from Passman et al 2023. Clonal CCO-deficient hepatocyte patches and nearby CCO-proficient hepatocytes were identified in morphologically normal human livers and sampled at varying distances along the PT-CV axis. Samples are named according to their location within the liver lobule, with "PT" denoting samples abutting the portal triad, "CV" denoting samples abutting the central hepatic vein, and "Mid" sampled acquired midway between these structures. Normal human liver is thought to be generally quiescent, however clonal hepatocyte expansions have been observed but neither their cellular source nor their expansion dynamics have been determined. Knowing the hepatocyte cell of origin, and their subsequent dynamics and trajectory within the human liver will provide an important basis to understand disease-associated dysregulation. Here we use in vivo lineage tracing and a combination of methylation sequence analysis to demonstrate normal human hepatocyte ancestry. We exploit next generation mitochondrial sequencing to determine hepatocyte clonal expansion dynamics across spatially-distinct areas of laser-capture microdissected clones, in tandem with computational modelling in morphologically-normal human liver.

| EGAS00001006984 | EGA

f5a3bc98-8b28-4a25-8b6d-5f10ef0fce80 - samples

Project description:BAM files containing paired-end mtDNA sequencing data from morphologically normal human liver. Clonal CCO-deficient patches of hepatocytes were identified in human liver samples, and samples were taken along a line spanning approximately from the portal triad to the central hepatic vein. Individual BAM files are named according to their patch, line and cut, where cut 1 is nearest to the portal triad, and cuts 2, 3 etc. lying further from the portal triad. Other file types include "Bulk" samples, contain sequencing data of the remaining CCO-deficient cells that were not sampled as part of the line of cuts, and "Stroma" control samples (used for identifying germ-line variants). Sequenced on NextSeq 500 platform.

| EGAD00001007991 | EGA

Transcription profiling by array of wheat after inoculation with Puccinia triticina, Puccinia hordei or mock-inoculation to identify candidate genes for nonhost resistance against rust disease

Project description:In this experiment the transcriptome reprogramming in wheat during host and nonhost interaction with Puccinia sp. was analyzed in a time-series approach. Ten days old wheat plants of cv. Renan were mock-inoculated or inoculated with P. triticina (Pt), BRW96258 isolate, or P. hordei (Ph), 1.2.1 isolate. After 12, 24, 36 and 48 hours first leaves were sampled. Total RNA was extracted using the RNeasy Plant Mini Kit (Qiagen, Hilden, Germany), the Ambion TURBO DNA-free DNase Kit was used for DNA elimination, and RNA was hybridized to Agilent 44k oligonucleotide arrays.

2017-12-02 | E-MTAB-5656 | biostudies-arrayexpress

Transcription profiling by array of barley after inoculation with Puccinia hordei, Puccinia triticina or mock-inoculation to identify candidate genes for nonhost resistance against rust disease

Project description:In this experiment the transcriptome reprogramming in barley during host and nonhost interaction with Puccinia sp. was analyzed in a time-series approach. Ten days old barley plants of cv. Vada were mock-inoculated or inoculated with P. hordei (Ph), 1.2.1 isolate, or P. triticina (Pt), BRW96258 isolate. After 12, 24, 36 and 48 hours first leaves were sampled. Total RNA was extracted using the RNeasy Plant Mini Kit (Qiagen, Hilden, Germany), the Ambion TURBO DNA-free DNase Kit was used for DNA elimination, and RNA was hybridized to Agilent 44k oligonucleotide arrays.

2017-12-02 | E-MTAB-5655 | biostudies-arrayexpress

Zebrafish liver: Tg(fabp10a:pt-beta-catenin) versus non-transgenic control siblings

Project description:To investigate mechanisms by which activated β-catenin signaling promotes liver tumor formation and to identify potential therapeutics for these cancers, we generated transgenic zebrafish expressing hepatocyte-specific activated β-catenin (Tg(fabp10a:pt-β-cat) zebrafish. As adults, these animals show increased liver size, decreased survival, and histologic abnormalities similar to human HCC. To further characterize our model, we used microarray analysis to compare gene expression in Tg(fabp10a:pt-β-cat) zebrafish livers to that of non-transgenic control sibling livers. This experiment includes 2 biological replicates. Each replicate represents one Tg(fabp10a:pt-beta-catenin) zebrafish compared to non-transgenic control sibling.

2015-04-30 | E-GEOD-68124 | biostudies-arrayexpress

Zebrafish liver: Tg(fabp10a:pt-beta-catenin) versus non-transgenic control siblings

2015-04-30 | GSE68124 | GEO

Disruption of Cytochrome c Oxidase Function Induces Warburg Effect and Metabolic Reprogramming

Project description:Defects in mitochondrial oxidative phosphorylation complexes, altered bioenergetics and metabolic shift are often seen in cancers. Here we show a role for the dysfunction of electron transport chain component, cytochrome c oxidase (CcO) in cancer progression. We show that genetic silencing of the CcO complex by shRNA expression and loss of CcO activity in multiple cell types from the mouse and human sources resulted in metabolic shift to glycolysis, loss of anchorage dependent growth and acquired invasive phenotypes. Disruption of CcO complex caused loss of transmembrane potential and induction of Ca2+/Calcineurin-mediated retrograde signaling. Propagation of this signaling, includes activation of PI3-kinase, IGF1R and Akt, Ca2+ sensitive transcription factors and also, TGF1, MMP16, periostin that are involved in oncogenic progression. Whole genome expression analysis showed up regulation of genes involved in cell signaling, extracellular matrix interactions, cell morphogenesis, cell motility and migration. The transcription profiles reveal extensive similarity to retrograde signaling initiated by partial mtDNA depletion, though distinct differences are observed in signaling induced by CcO dysfunction. The possible CcO dysfunction as a biomarker for cancer progression was supported by data showing that esophageal tumors from human patients show reduced CcO subunits IVi1 and Vb in regions that were previously shown to be hypoxic core of the tumors. Our results show that mitochondrial electron transport chain defect initiates a retrograde signaling. These results suggest that a defect in CcO complex can potentially induce tumor progression.

2015-05-05 | GSE68525 | GEO

HMGB1 signaling phosphorylates Ku70 and impairs DNA damage repair in Alzheimer’s disease pathology

Project description:DNA damage is increased in Alzheimer’s disease (AD), while the underlying mechanisms are unknown. Here, we employ comprehensive phosphoproteome analysis, and identify abnormal phosphorylation of 70 kDa subunit of Ku antigen (Ku70) at Ser77/78, which prevents Ku70-DNA interaction, in human AD postmortem brains. The abnormal phosphorylation inhibits accumulation of Ku70 to the foci of DNA double strand break (DSB), impairs DNA damage repair and eventually causes transcriptional repression-induced atypical cell death (TRIAD). Cells under TRIAD necrosis reveal senescence phenotypes. Extracellular high mobility group box 1 (HMGB1) protein, which is released from necrotic or hyper-activated neurons in AD, binds to toll-like receptor 4 (TLR4) of neighboring neurons, and activates protein kinase C alpha (PKCα) that executes Ku70 phosphorylation at Ser77/78. Administration of human anti-HMGB1 antibody to post-symptomatic AD model mice decreases neuronal DSBs, suppresses secondary TRIAD necrosis of neurons, prevents escalation of neurodegeneration, and ameliorates cognitive symptoms. TRIAD shares multiple features with senescence. These results newly unravel the HMGB1-Ku70 axis that accounts for the increase of neuronal DNA damage and secondary enhancement of TRIAD, the cell death phenotype of senescence, in AD.

2022-02-15 | PXD028089 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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