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Effect of treatment with 5uM of the type I PRMT inhibitor MS023 dissolved in DMSO for 3 days and of a stably transduced PRMT1 specific dox-inducible knockdown over 4 days in ccRCC cell line models RCC243 and 786-0

ABSTRACT: Effect of treatment with 5uM of the type I PRMT inhibitor MS023 dissolved in DMSO for 3 days and of a stably transduced PRMT1 specific dox-inducible knockdown over 4 days in ccRCC cell line models RCC243 and 786-0

PROVIDER: PRJNA954060 | ENA |

REPOSITORIES: ENA

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Effect of treatment with 5uM of the type I PRMT inhibitor MS023 dissolved in DMSO for 3 days and of a stably transduced PRMT1 specific dox-inducible knockdown over 4 days in ccRCC cell line models RCC243 and 786-0

Project description:To investigate the effect of pharmacological inhibition of the type I PRMTs in ccRCC cell lines. We treated one patient derived cell line (RCC243) and one commercially available line (786-0) in duplicate with 5uM MS023 for 3 days vs. 0.1% DMSO alone. We then performed gene expression profiling analysis using data obtained from RNA-seq. Each cell line was treated as a biological replicate. Similarly, to investigate the genetic knockdown of PRMT1 using the same cell lines, stably transduced dox-inducible PRMT1 targeting shRNA's. Cell lines were treated with or with out 1ug/mL dox for 4 days in triplicate. Gene expression profiling analysis was then performed using data obtained from RNA-seq.

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786-O and 786-VHL in EMCV study

Project description:786-0 is a cell line derived from a clear cell renal carcinoma. Previous studies have shown that the 786-O cell line harbors an inactivating mutation in the von-Hippel Lindau (VHL) gene. Mutations in the VHL gene occur in the majority of sporadic clear cell renal cell. To determine how inactivation of the VHL affects cellular functions, we created a derivative of 786-0, which we call 786-VHL in which a functional allele of VHL has been introduced back into the 786-O cell line. The renal cell carcinoma cell line 786-0, which harbors a mutated allele of VHL, was compared to a cell line derived from 786-0, termed 786-VHL, that contains a functional allele of VHL. Genes whose expression characteristics were dependent on functional VHL were identified.

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786-O and 786-VHL in EMCV study

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Type I PRMT inhibitor MS023 promotes SMN2 exon 7 inclusion and synergizes with nusinersen to rescue the phenotype of SMA mice

Project description:In our study we have identified MS023, an inhibitor of PRMTs, to increase SMN protein and FL SMN2 transcript levels, and to improve survival and weights of treated SMA mice, alone and in combination with currently approved antisense oligonucleotide. In order to understand the molecular underpinnings of the added benefit provided by the combinatorial treatment, we performed bulk transcriptomic analysis in spinal cords of SMA mice treated with MS023 only, nusinersen only, and MS023 in combination with nusinersen, compared to wild type and SMA littermates.

2023-03-01 | GSE206400 | GEO

RNA-seq of murine small intestinal organoids treated with type I PRMT inhibitor MS023 against untreated controls

Project description:Murine small intestinal organoids were cultured in the presence or absence of 5µM inhibitor MS023 (PubChem CID 92136227), which targets type I protein arginine methyltransferases Prmt1, Prmt3, Prmt4, Prmt6, Prmt8. Organoids were grown in culture media containing EGF, Noggin and R-spondin (ENR), media was changed after 48h, and organoids were harvested after 120h.

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Histone arginine methylation by Prmt controls lung branching morphogenesis through transcriptional repression of Bmp

Project description:We report that a protein arginine methyltransferase Prmt and symmetric dimethylation at histone H arginine (HRsme) directly associates with chromatin of Bmp to suppress its transcription. Inactivation of Prmt in the lung epithelium results in halted branching morphogenesis, altered P-D airway patterning and neonatal lethality.

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Arginine Methylation Regulates SARS-CoV-2 Nucleocapsid Protein Function and Viral Replication

Project description:Viral proteins are known to be methylated by host protein arginine methyltransferases (PRMTs) playing critical roles during viral infections. Herein, we show that PRMT1 methylates SARS-CoV-2 nucleocapsid (N) protein at residues R95 and R177 within RGG/RG sequences. Arginine methylation of N protein was confirmed by immunoblotting viral proteins extracted from SARS-CoV-2 virions isolated by cell culture. We demonstrate that arginine methylation of N protein is required for its RNA binding capacity, since treatment with a type I PRMT inhibitor (MS023) or substitution of R95K or R177K inhibited interaction with the 5’-UTR of the SARS-CoV-2 genomic RNA. We defined the N interactome in HEK293 cells with or without MS023 treatment and identified PRMT1 and many of its RGG/RG substrates including the known interactor, G3BP1, and other components of stress granules (SG). Methylation of N protein at R95 regulates another function namely its property to suppress the formation of SGs. MS023 treatment or R95K substitution blocked N-mediated suppression of SGs. Also, the co-expression of methylarginine reader TDRD3 quenched N-mediated suppression of SGs in a dose-dependent manner. Finally, pre-treatment of VeroE6 cells with MS023 significantly reduced SARS-CoV-2 replication. With type I PRMT inhibitors being in clinical trials for cancer treatment, inhibiting arginine methylation to target the later stages of the viral life cycle such as viral genome packaging and assembly of virions may be an additional therapeutic application of these drugs.

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RNA-seq of murine small intestinal organoids treated with type I PRMT inhibitor MS023 against untreated controls

Project description:RNA-seq of murine small intestinal organoids treated with type I PRMT inhibitor MS023 against untreated controls

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Expression profile of human 786-O cells overexpressing Bcl-xAS lncRNA

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2021-03-02 | GSE38766 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of 786-O and sunitinib resistant 786-O (7R) cell lines

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare the different gene between 786-O and 7R cell lines

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