Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

ABSTRACT: Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

PROVIDER: PRJNA660481 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12558816.fastq.gz	Fastqsanger.gz
	SRR12558817.fastq.gz	Fastqsanger.gz
	SRR12558818.fastq.gz	Fastqsanger.gz
	SRR12558819.fastq.gz	Fastqsanger.gz
	SRR12558820.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

Project description:Rationale: RNA binding protein Apobec1 Complementation Factor (A1CF) regulates posttranscriptional ApoB mRNA editing but the range of RNA targets and long-term impact of altered A1CF expression on liver function are unknown. Objective: We studied hepatocyte-specific A1cf transgenic (A1cf +/Tg), A1cf+/Tg Apobec1– /– and A1cf –/– mice fed chow or high fat/high fructose diets using RNA-Seq, RNA-CLIP Seq and tissue microarrays from human hepatocellular cancer (HCC). Findings: A1cf +/Tg mice exhibited increased hepatic proliferation and steatosis, with increased lipogenic gene expression (Mogat1, Mogat2, Cidea, Cd36) associated with shifts in polysomal RNA distribution. Aged A1cf +/Tg mice developed spontaneous fibrosis, dysplasia and HCC, which was accelerated on a high fat/fructose diet and independent of Apobec1. RNA-Seq revealed increased expression of mRNAs involved in oxidative stress (Gstm3, Gpx3, Cbr3), inflammatory response (Il19, Cxcl14, Tnfα, Ly6c), extracellular matrix organization (Mmp2, Col1a1, Col4a1), proliferation (Kif20a, Mcm2, Mcm4, Mcm6) with a subset of mRNAs (including Sox4, Sox9, Cdh1) identified in RNA CLIP-Seq. Increased A1CF expression in human HCC correlated with advanced fibrosis and with reduced survival in a subset with nonalcoholic fatty liver disease. Conclusions: Hepatic A1CF overexpression selectively alters polysomal distribution and mRNA expression, promoting lipogenic, proliferative and inflammatory pathways leading to HCC.

2020-09-01 | GSE157233 | GEO

Comparative gene expression profiling in livers of A1cf-transgenic and wild-type mice

2020-09-05 | GSE157516 | GEO

Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

Project description:Purpose: A1CF is an RNA binding protein that has not been extensively studied on a transcriptome-wide scale. Here we profile the livers of wild-type and A1cf knockout mice to detect differences in gene expression. Methods: mRNA profiles of 6-8 week old wild-type and A1cf knockout mice were generated by deep sequencing using Illumina HiSeq 2500. Reads that passed quality filters were aligned to mm10 genome and analyzed for differential expression using CuffDiff2 and DESeq2. Results: We mapped reads to the mm10 genome and found a subset of fewer than 500 differentially expressed genes in A1CF deficiency. Conclusions: Our study represents the first transcriptomic profiling of A1CF deficiency in the liver.

2019-10-31 | GSE108547 | GEO

Comparative gene expression profiling in livers of A1cf-transgenic and wild-type mice

Project description:Comparative gene expression profiling in livers of A1cf-transgenic and wild-type mice

| PRJNA661555 | ENA

Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

Project description:Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

| PRJNA427593 | ENA

Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Whole Kidneys

Project description:Purpose: A1CF is an RNA binding protein that has not been extensively studied on a transcriptome-wide scale. Here we profile the whole kidneys of wild-type and A1cf knockout mice to detect differences in gene expression. Methods: mRNA profiles of 6-8 week old wild-type and A1cf knockout mice were generated by deep sequencing using Illumina HiSeq 2500. Reads that passed quality filters were aligned to mm10 genome and analyzed for differential expression using CuffDiff2 and DESeq2. Results: We mapped reads to the mm10 genome and found a subset of fewer than 500 differentially expressed genes in A1CF deficiency. Conclusions: Our study represents the first transcriptomic profiling of A1CF deficiency in the kidney.

2019-07-01 | GSE108548 | GEO

Interactomics Analyses of Wild-type and Mutant A1CF Reveal Diverged Functions in Regulating Cellular Lipid Metabolism

Project description:Population genetic studies highlight a missense variant (G398S) of A1CF that is strongly associated with higher levels of blood triglycerides (TGs) and total cholesterol (TC). Functional analyses suggest that the mutation accelerates the secretion of very low-density lipoprotein (VLDL) from the livers by an unknown mechanism. Here, we used multi-omics approaches to interrogate the functional difference between the WT and mutant A1CF. Using metabolomics analyses, we captured the cellular lipid metabolite changes induced by the transient expression of the proteins, confirming that the mutant A1CF is able to relieve the TG accumulation induced by WT A1CF. Using a proteomics approach, we obtained the interactomic data of WT and mutant A1CF. Networking analyses show that WT A1CF interacts with three functional protein groups, RNA/mRNA processing, cytosolic translation and, surprisingly, mitochondrial translation. The mutation diminishes these interactions, especially with the group of mitochondrial translation. Differential analyses show that the WT A1CF-interacting proteins most significantly different from the mutant are those for mitochondrial translation, whereas the most significant interacting proteins with the mutant are those for cytoskeleton and vesicle-mediated transport. RNA-seq analyses validate that the mutant, but not the WT, A1CF increases the expression of the genes responsible for cellular transport processes. On the contrary, WT A1CF affected the expression of mitochondrial matrix proteins and increased cell oxygen consumption. Thus, our studies confirm the previous hypothesis that A1CF plays broader roles in regulating gene expression. The interactions of the mutant A1CF with the vesicle-mediated transport machinery provide mechanistic insight in understanding the increased VLDL secretion in the A1CF mutation carriers.

2022-06-30 | GSE152807 | GEO

Hepatocypte-specific Caveolin-1 knockout livers

Project description:Hepatocypte-specific Caveolin-1 knockout livers

| PRJNA565232 | ENA

Mouse livers: control vs miR-155 transgenic mice

Project description:Transcriptional profiling of mouse livers comparing control mice with miR-155 transgenic mice that overexpression of miR-155 in the liver

2017-02-09 | GSE64255 | GEO

Wild type and Neuregulin 4 (Nrg4) knockout (KO) mouse livers

Project description:Nrg4 is a brown fat-enriched adipokine that binds to the liver and suppress the process of steatosis-to-NASH progression. Adipose tissue Nrg4 expression was reduced in mice under NASH diet feeding. Nrg4 homozygous knockout mice are prone to diet-induced steatohepatitis We used microarrays to elucidate the pathogenic pathways that are regulated by Nrg4 deficiency in the livers of mice under NASH diet feeding.

2018-02-14 | GSE99753 | GEO

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