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Next generation sequencing comparing effects of FFSS, FAK inhibitor and FAK gene deletion. [FFSS]

ABSTRACT: Purpose: The goals of this study are to compare the effect of FFSS, HDAC4 and HDAC5 gene deletion on gene expression of NGS-derived RNA-sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE144265 | GEO | 2020/01/28

REPOSITORIES: GEO

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Next generation sequencing comparing effects of FFSS, FAK inhibitor and FAK gene deletion.

Project description:Purpose: The goals of this study are to compare the effect of FFSS, FAK inhibitor, and FAK gene deletion on gene expression of NGS-derived RNA-sequencing.

2019-10-31 | GSE139604 | GEO

Next generation sequencing comparing effects of FFSS, FAK inhibitor and FAK gene deletion. [FFSS]

Project description:Next generation sequencing comparing effects of FFSS, FAK inhibitor and FAK gene deletion. [FFSS]

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Next generation sequencing comparing effects of FFSS, FAK inhibitor and FAK gene deletion.

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Next generation sequencing comparing effects of vehicle, PTH, and YKL-05-093 in Ocy454 cells

Project description:Purpose: The goals of this study are to compare the effects of vehicle, PTH, and YKL-05-093 on gene expression by NGS-derived RNA-sequencing Methods: Ocy454 cells were grown at 37C for 14 days . Cells were then treated with vehicle, PTH (1 nM), or YKL-05-093 (0.5 uM) for 4 hours. Total RNA was isolated using Qiagen Rneasy columns, and submitted for NGS library generation and sequencing. All experiments performed in duplicate.

2016-09-06 | E-GEOD-76932 | biostudies-arrayexpress

Next generation sequencing comparing effects of vehicle, PTH, and YKL-05-093 in Ocy454 cells

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Transcriptome analysis of satellite cells with a genetic deletion of HDAC4 to identify the gene modulated by HDAC4

Project description:NGS technology was used for high-throughput profiling of the transcriptome by comparing satellite cells lacking or not HDAC4.

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FAK activity alters the transcriptional landscape during SMC phenotypic switching

Project description:Purpose: The goals of this study are to compare the effect of FAK activity on gene expression of NGS-derived RNA-sequencing during vascular remodeling.

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Class IIa HDACs reprogram mitochondrial metabolism to inhibit apoptosis and ferroptosis in response to lipotoxicity

Project description:Lipotoxicity, the accumulation of lipids in non-adipose tissues, alters the metabolic transcriptome and mitochondrial metabolism in skeletal muscle. The mechanisms involved remain poorly understood. Here we show that lipotoxicity increased histone deacetylase 4 (HDAC4) and histone deacetylase 5 (HDAC5), which reduced the expression of metabolic genes and oxidative metabolism in skeletal muscle. This metabolic reprogramming was linked with reduced expression of p53-dependent genes that mediate apoptosis and ferroptosis, which preserved cell viability in response to lipotoxicity. Mechanistically, impaired mitochondrial metabolism reduced acetylation of p53 at K120, a modification required for transcriptional activation of apoptosis, while redox drivers of ferroptosis were also reduced. Overexpression of loss-of-function HDAC4 and HDAC5 mutants in skeletal muscle of obese db/db mice enhanced oxidative capacity, increased apoptosis and ferroptosis and reduced muscle mass. This study identifies HDAC4 and HDAC5 as repressors of the oxidative state of skeletal muscle, and that this metabolic reprogramming, considered deleterious for normal metabolism, is critical to preserve muscle integrity in response to lipotoxicity.

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Protein expression profiling of human urothelial carcinoma cell lines RT-112, VM-Cub-1, SW1710, UMUC3 and a benign urothelial control HBLAK engineered to stably express HDAC5 against their vector control

Project description:Aberrant expression of histone deacetylases (HDACs) and their activity are associated with a broad range of tumor development. However, based on cell or tissue types, class IIA HDACs such as HDAC4 and HDAC5 may facilitate or inhibit cancer progression. The goal of this project is to examine the overall proteome changes caused by HDAC5 expression. Here, we studied the effects of stable expression of HDAC5 (that is normally downregulated or have a weak basal expression) in four urothelial carcinoma (UC) cell lines (RT112, VM-Cub-1, SW1710, and UM-UC-3) by mass spectrometry in comparison to their vector controls. We observed that HDAC5 expression in VM-Cub-1 triggered a drastic phenotype change from an epitheloid to a mesenchymal (i.e., epithelial-mesenchymal transition, EMT) and altogether diminished cell proliferation of the other three cell lines. Our mass-spec data are in line with the phenotypic transformation of VM-Cub-1. In addition, we also performed a protein expression profiling of HBLAK, a spontaneously immortalized from primary human bladder epithelial cells that can be directly compared with the four UC vector cells. HBLAK vector cells only were included for mass-spec as the cells failed to express HDAC5 after lentiviral transduction and selection.

2022-03-14 | PXD014448 | Pride

RNAseq data comparing HDAC5 eccaper PDAC cells with HDAC5 knockdown and scramble control

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2020-04-27 | GSE149127 | GEO

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