Transcriptome sequencing of skeletal muscle for PRMT7 knockout mouse
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE75993 | GEO | 2016/01/01
SECONDARY ACCESSION(S): PRJNA305921
REPOSITORIES: GEO
Similar Datasets
Project description:We report that whole body PRMT7-/- adult mice display a significant reduction in in muscle mass. RNA sequencing was performed to identify potential PRMT7 targets. We found that top canonical pathways affected by the loss of PRMT7 includes cell cycle and senescence. RNA was extracted from tibialis anterior muscles harvested from 3 WT and 3 PRMT7 null mice at 8months. RNA sequencing was performed to compare mRNA in skeletal muscles between WT and KO mice.
2016-07-03 | E-GEOD-75993 | biostudies-arrayexpress
Project description:Protein arginine methyltransferases (PRMTs) regulate diverse biological processes and are increasingly being recognized for their potential as drug targets. Here we report the discovery of a potent, selective and cell active chemical probe for PRMT7. SGC3027 is a cell permeable prodrug, which in cells, is converted to SGC8158, a potent, SAM-competitive PRMT7 inhibitor. Inhibition or knockout of cellular PRMT7 resulted in drastically reduced levels of monomethylation of HSP70 family members and other stress-associated proteins. Structural and biochemical analysis revealed that PRMT7-driven in vitro methylation of HSP70 at R469 requires an ATP-bound, open conformation of HSP70. In cells, SGC3027 inhibited methylation of both, constitutive and inducible forms of HSP70, and led to decreased tolerance for perturbations in proteostasis. These results demonstrate a role for PRMT7 in stress response. SGC3027 is the first chemical probe for PRMT7 and together with its inactive control SGC3027N, will be valuable chemical tools to further investigate the role of PRMT7 in human health and disease.
2022-02-23 | PXD012119 | Pride
Project description:To explore the mechanism by which PRMT7 regulates HCC cell malignant phenotypes, we performed RNA-seq in QGY-7703 cells before and after PRMT7 knockdown to identify the affected signaling pathways. 296 differentially expressed genes were identified in PRMT7-downregulated cells (Figure 6A) and these genes were enriched in cancer-related pathways including MAPK signaling pathway, p53 signaling pathway, and FoxO signaling pathway (Figure 6B), as revealed by DAVID KEGG analysis.
2021-02-25 | GSE167432 | GEO
Project description:Under inflammatory conditions the extravasation of monocytes into tissues through trans-endothelial migration is a fundamental immunological process underlying innate inflammatory responses across multiple organ systems contributing to tissue injury and the progression of autoimmunity, cardiovascular disease and particularly chronic lung disease. Methylation of protein arginine residues via protein arginine methyltransferases (PRMTs) is a post-translational epigenetic modification implicated in inflammatory responses. How PRMTs, particularly PRMT7, epigenetically regulates monocyte-driven inflammatory response in disease remains unclear. Here, we perform ATAC-seq analysis on an MHS macrophage cell line in which PRMT7 has been disrupted by CRISPR/Cas9 to examine chromatin accessibility regulated by PRMT7.
2022-01-12 | GSE153666 | GEO
Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with only few established prognostic biomarkers.In this study, we examined the expression of protein arginine methyltransferases across hematological malignancies and discovered high levels of PRMT7 mRNA in T-ALL, particularly in the mature subtypes of T-ALL. High PRMT7 was associated with decreased event-free and overall survival in two independent patient cohorts. Genetic deletion of PRMT7 by CRISPR-Cas9 significantly decreased the colony-forming capacity of the cells and negatively impacted cell viability. In the knockout cells, alterations were seen in the monomethyl arginine levels in proteins associated with RNA processing. These results suggest that PRMT7 plays an active role in T-ALL pathogenesis.
2021-10-22 | GSE186238 | GEO
Project description:Purpose: RNA-sequencing analysis defined a novel role for PRMT7 in melanoma cancer immunotherapy. Methods: PRMT7-deficient cells and control B16.F10 cells treated with mIFN-γ (100ng/ml) for 24 hours. B16.F10 melanoma cells mRNA profiles were generated by deep sequencing, in triplicate using TruSeq Stranded mRNA Sample Prep Kit with TruSeq Unique Dual Indexes (Illumina, Hiseq4000, SR75 platform located at San Diego, CA; UCSD IGM Genomics Facility, La Jolla, CA). Resulting libraries were multiplexed and sequenced with 100 base pair (bp) to a depth of approximately 30 million reads per sample. The sequence reads that passed quality filters were trimmed with Trimmomatic v0.39. STAR v2.7.1a was then used to align the reads to the mouse genome (mm10/GRCm38). Gene expression was quantified across all samples with HOMER v4.11.1, and the normalization was carried out through the regularized logarithm (rlog) transformation of DESeq2 v1.26.0. Differential expression between PRMT7 WT and knockdown samples were calculated through DESeq2 v1.26.0, and the gene expression was considered significantly different if the absolute value of the log-fold-change (LFC) was higher than 2, the base means larger than 10 and the false discovery rate (FDR) less than 0.05. Results: Differential expression analysis between the siLuc and siPRMT7 conditions yielded 185 and 251 genes with statistically significant differences and absolute fold change greater than 2 in the IFN– and IFN+ treatments respectively. Of these, 85% of genes are upregulated in the IFN– treatment, while 72% of genes are downregulated in the IFN+ treatment. Gene ontology analysis using the 185 and 251 lists of differentially expressed genes implies that the downregulated biological processes are enriched for the immune response pathways, while upregulated genes are more involved in the cell cycle process. Altered expression of some genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to better understand PRMT7 function in cancer immunotherapy. Conclusions: Our study represents the first detailed analysis of B16.F10 melanoma transcriptomes without PRMT7 expression, with biologic replicates, generated by RNA-seq technology. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of PRMT7 biologic functions in modulating melanoma transcriptome.
2022-03-01 | GSE157141 | GEO
Project description:PRMT7 regulated chromatin accesibility in myeloid cells [ATAC-Seq]
| PRJNA643578 | ENA
Project description:Effects of Prmt7 genetic deletion to arginine monomethylation in Jurkat T-ALL cell line. Analysis was made using two different Prmt7 KO and one control cell lines.
2022-03-28 | PXD032819 | JPOST Repository
Project description:Autophagy deficient melanocytes display a senescence associated secretory phenotype that includes oxidized lipid mediators
| PRJNA327211 | ENA
Project description:Apigenin, a natural flavone abundant in various plant-derived foods including parsley and celery, has been shown to prevent inflammation and inflammatory diseases. However, the effect of apigenin on skeletal muscle hypertrophy and myogenic differentiation has not previously been elucidated. Here, we investigated the effects of apigenin on quadricep muscle weight and running distance using C57BL/6 mice on an accelerating treadmill. Apigenin stimulated mRNA expression of MHC (myosin heavy chain) 1, MHC2A, and MHC2B in the quadricep muscles of these animals. GPR56 (G protein-coupled receptor 56) and its ligand collagen III were upregulated by apigenin supplementation, together with enhanced PGC-1?, PGC-1?1, PGC-1?4, IGF1, and IGF2 expression. Prmt7 protein expression increased in conjunction with Akt and mTORC1 activation. Apigenin treatment also upregulated FNDC5 (fibronectin type III domain containing 5) mRNA expression and serum irisin levels. Furthermore, apigenin stimulated C2C12 myogenic differentiation and upregulated total MHC, MHC2A, and MHC2B expression. These events were attributable to an increase in Prmt7-p38-myoD expression and Akt and S6K1 phosphorylation. We also observed that Prmt7 regulates both PGC-1?1 and PGC-1?4 expression, resulting in a subsequent increase in GPR56 expression and mTORC1 activation. Taken together, these findings suggest that apigenin supplementation can promote skeletal muscle hypertrophy and myogenic differentiation by regulating the Prmt7-PGC-1?-GPR56 pathway, as well as the Prmt7-p38-myoD pathway, which may contribute toward the prevention of skeletal muscle weakness.
| S-EPMC5667963 | biostudies-literature