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ABSTRACT: Differential splicing analysis of liver-specific A1cf knock-out mice

PROVIDER: PRJNA530736 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8842341.fastq.gz	Fastqsanger.gz
	SRR8842342.fastq.gz	Fastqsanger.gz
	SRR8842343.fastq.gz	Fastqsanger.gz
	SRR8842344.fastq.gz	Fastqsanger.gz
	SRR8842345.fastq.gz	Fastqsanger.gz

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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: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.

2020-09-05 | GSE157516 | GEO

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

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Loss of canonical splicing factor SRSF1 in hepatocytes results in acute liver injury and regeneration

Project description:Post-transcriptional gene regulatory mechanisms (PTGRM) contribute profoundly to liver development and physiology. Alternative splicing is one of the earliest mechanisms of gene regulation acting on nascently transcribed mRNA. This process is mediated by a large class of proteins known as splicing factors. SRSF1 is a canonical splicing factor with roles in both constitutive and alternative splicing. While its biochemical activities have been studied extensively, its role in tissue physiology are not well defined. In this study we investigate the role of SRSF1 in liver physiology using hepatocyte-specific knock-out mice models. Hepatocyte-specific knock-out of SRSF1 was achieved in two ways; 1) SRSF1 floxed mice were crossed with AlbCre transgenic mice and 2) SRSF1 floxed mice were injected with AAV8-TBG-iCre viral vector. The latter model allowed for investigating acute changes in hepatocyte upon ablation of SRSF1. Both models exhibit acute liver injury with severe cellular damage, inflammation and lipid accumulation. Utilizing high-throughput transcriptome profiling on purified hepatocytes, we find acute loss of SRSF1 triggers activation of the p53 pathway and splicing dysregulation of genes involved in mRNA metabolism. Continuous hepatic injury in this model eventually triggers a regenerative response resulting in the upregulation of genes involved in proliferation and repopulation of the tissue parenchyma.

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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.

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Larp7 Knock-out Staged Male Germ Cells Transcriptomes

Project description:Analysis the difference in the transcriptomes (expression and alternative splicing) of either spermatocytes or round spermatids between Larp7 conditional knock-out and control mice

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Project description:Differential expression of miRNA in Tax1BP1 knock-out mice [miRNA]

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