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Expression of genes in HepG2 cells with Knock-out in cholesterol synthesis

ABSTRACT: Expression of genes in HepG2 cells with Knock-out in cholesterol synthesis

PROVIDER: PRJNA915029 | ENA |

REPOSITORIES: ENA

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Expression of genes in HepG2 cells with Knock-out in cholesterol synthesis

Project description:HepG2 cell line CRISPR-Cas9 generated Knock-out in 4 cholesterol synthesis gene: CYP51, DHCR24, SC5D and HSD17B7 Excess of cholesterol associates with a variety of diseases so its synthesis must be under tight homeostatic control. The early part of cholesterol synthesis with rate-limiting HMGCR and SQLE steps is proceeded by the sterol part where numerous non-polar sterols with poorly defined biological functions are produced. To illuminate their role we developed knockouts (KO) for the consecutive enzymes that metabolize sterols towards cholesterol CYP51A1, DHCR24, SC5D resulted in the accumulation of specific set of sterols in each KO cell. Despite that, we targeted three steps of the cholesterol synthesis housekeeping pathway, the overlap of de-regulated genes was only 9%, suggesting that each set of sterols modulated the hepatic cell transcriptome uniquely. Lanosterol and 24,25-dihydrolanosterol, but not other non-polar sterols, provoked higher cell proliferation, cell cycle changes, and upregulation of metabolic pathways and transcription factors (TFs) associated with cancer progression and immune response like NFKB, SMAD, ESR1 and highly elevated LEF1 a protein from WNT signalling. In contrast, lathosterol and desmosterol caused slower proliferation and apoptosis promotion, through TFs like HNF1A and E2F. We were able to show how sterols from early part of synthesis can promote cell proliferation as sterols from end of synthesis suppress proliferation. These findings challenge the current dogma that sterols produced during cholesterol synthesis have similar biological functions

2024-08-08 | GSE221582 | GEO

LDLR and HMGCR double knock out human HepG2 cells LC-MSMS

Project description:Our study focuses on searching for novel genes involved in cholesterol metabolism through genome-wide screening, RNA-seq, proteome and lipidomic.This project maily focus on the proteomics of LDLR and HMGCR double knock out human HepG2 cells.

2025-02-24 | PXD052324 | Pride

The effects of knock-out PARP1 on HepG2.

Project description:The effects of knock-out PARP1 on HepG2.

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Up-regulation of cholesterol synthesis pathways and neurodegeneration in a knock-in Sod1 mutant mouse model of ALS.

Project description:Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disorder affecting brain and spinal cord motor neurons. Mutations in the copper/zinc superoxide dismutase gene (SOD1) are associated with ~20% of inherited and 1-2% of sporadic ALS cases. Much has been learned from mice expressing transgenic copies of mutant SOD1, which typically involve high-level transgene expression, thereby differing from ALS patients expressing one mutant gene copy. We created a knock-in point mutation in the endogenous mouse Sod1 gene leading to mutant SOD1G85R protein expression, a human ALS-causing mutation, to generate a model that more closely represents patient gene expression. Heterozygous Sod1G85R mutant mice resemble wild type, whereas homozygous mutants have reduced body weight and lifespan, a mild neurodegenerative phenotype, and express very low mutant SOD1 protein levels with no detectable SOD1 activity. Homozygous mutants exhibit partial neuromuscular junction denervation at 3-4 months of age. Spinal cord motor neuron transcriptome analyses of homozygous Sod1G85R mice revealed up-regulation of cholesterol synthesis pathway genes compared to wild type. Transcriptome and phenotypic features of these mice are similar to Sod1 knock-out mice, suggesting the Sod1G85R phenotype is largely driven by loss of SOD1 function. By contrast, cholesterol synthesis genes are down-regulated in severely affected human TgSOD1G93A transgenic mice at 4 months. Our analyses implicate dysregulation of cholesterol or related lipid pathway genes in ALS pathogenesis. The Sod1G85R knock-in mouse is a useful ALS model to examine the importance of SOD1 activity in control of cholesterol homeostasis and motor neuron survival.

2026-05-01 | GSE231531 | GEO

Transcriptome network analysis of Smug1 knock-out cells by using CRISPR/Cas9 system

Project description:Purpose: To build a differential transcriptome network in Smug1 knock-out HepG2 hepatocarcinoma cells. Methods: Transcriptome analysis by the RNA-seq via mRNA pull-down. Results: We constructed transcriptome from Smug1 knock-out cells by using RNA-seq analysis. Nucleosome and miRNA related genes were highly enriched in Smug1 KO HepG2 cells. Conclusions: Smug1 regulate the gene expression related with nucleosome assembly and histone function.

2020-06-30 | GSE145210 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of control, SETD6 Knock-out, SETD3 knock-out and SETD6+SETD3 knock-out HeLa cells Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of control, SETD6 Knock-out, SETD3 knock-out and SETD6+SETD3 knock-out HeLa cells Transcriptomes

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ARRDC4 knock out Mouse Heart Analysis

Project description:ARRDC4 knock out Mouse Heart Analysis

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anaerobic knock-out

Project description:Six different knock-out strains' expression data under anaerobic condition Keywords: parallel sample

2004-03-10 | GSE1107 | GEO

aerobic knock-out

Project description:Six different knock-out strains' expression data under aerobic condition Keywords: parallel sample

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GNPS - Stieleria Neptunia Enr13 Stieleriacines D-E + knock out studies, Total Synthesis Stieleriacine C + derivatives

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