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Evaluation of splicing alterations in mice treated with RECTAS.

ABSTRACT: Evaluation of splicing alterations in mice treated with RECTAS.

PROVIDER: PRJNA843989 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19450600_1.fastq.gz	Fastqsanger.gz
	SRR19450600_2.fastq.gz	Fastqsanger.gz
	SRR19450601_1.fastq.gz	Fastqsanger.gz
	SRR19450601_2.fastq.gz	Fastqsanger.gz
	SRR19450602_1.fastq.gz	Fastqsanger.gz

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Evaluation of splicing alterations in mice treated with RECTAS.

Project description:Aberrant pre-mRNA splicing events in tumor cells generate tumor-specific splice junctions, translating potential neoantigens. RNA-seq was performed to examine whether a small molecule compound RECTAS affect splice patterns followed by neoantigen repertoire in mouse colon, lung, and liver tissues.

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Evaluation of coloncyte genes in TNBS-induced colitis mice treated with I3C

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Splicing changes in gastrocnemius muscle from 3-month-old HSALR mice

Project description:The initial aim of the study was to determine the mechanisms underlying the positive effect of AICAR on the phenotype of HSALR mice, a well-known model for DM1. We have previously shown that treatment with AICAR reduces myotonia and mis-splicing in the HSALR mice. We here aimed to identify splicing and transcriptional changes in gastrocnemius muscle from HSALR mice treated or not with AICAR, as compared to FVB control mice. The data obtained from untreated mice were then used in the study focused on NMJ alterations and CaMKII deregulation in DM1.

2024-06-06 | GSE226676 | GEO

To identify alterations induced in gastric mucosa of mice exposed to Pteridium aquilinum and/or infected with Helicobacter pylori

Project description:The aim of this study is to identify alterations induced in gastric mucosa of mice exposed to Pteridium aquilinum and/or infected with Helicobacter pylori, in order to identify genes that are induced by bracken fern exerts exacerbating effects on gastric lesions associated to the infection. Six groups of C57Bl/6 mice were be used: 1) control, 2) infected Helicobacter pylori, 3) treated with Bracken fern extract orogastrically, 4) treated with Bracken fern extract in drinking water, 5) infected Helicobacter pylori + treated with Bracken fern extract orogastrically, 6) infected Helicobacter pylori + treated with Bracken fern extract in drinking water. The infection procedure was performed using an orogastric inoculation of H.pylori (strain SS1) twice in the first week. The RNA isolation was done in triplicate (3 mice per each condition). Further evaluation of morphological alterations on gastric mucosa, proliferative index and induction of DNA strand breaks will be performed in the mice stomach exposed to Pteridium aquilinum infected or not with Helicobacter pylori. Alterations of glycosylation in gastric tissues will also evaluated.

2011-09-07 | E-GEOD-31991 | biostudies-arrayexpress

Expression alterations in vildagliptin treated rats arota

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Alterations in alternative RNA splicing in hepatocytes from high-fat diet fed C57BL/6 male mice

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Influenza virus infection induces widespread alterations of host cell splicing

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Ablation of the epithelial-specific splicing factor Esrp1 results in ureteric branching defects and reduced nephron number

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Misregulation of alternative splicing of BIN1 leads to T-tubule alterations and muscle weakness in myotonic dystrophy

Project description:Myotonic dystrophes (DM), the most common adult muscular dystrophy, are the first recognized examples of RNA-mediated diseases in which expression of mutant RNAs containing expanded CUG or CCUG repeats interfere with the splicing of other mRNAs. Using whole-genome microarrays, we found that alternative splicing of the BIN1 mRNA is altered in DM skeletal muscle tissues, resulting in the expression of an inactive form of BIN1 deprived of phosphoinositide-binding and membrane-tubulating activities. BIN1 is involved in tubular invaginations of the plasma membrane and is essential for biogenesis of the muscle T-tubules, which are specialized skeletal muscle membrane structures essential to correct excitation-contraction (E-C) coupling. Mutations in the BIN1 gene cause centronuclear myopathy (CNM) that shares some histopathological features with DM, and both diseases are characterized by muscle weakness. Consistent with a loss-of-function of BIN1, muscle T-tubules were altered in DM patients, and membrane tubulation was restored upon expression of the correct splicing form of BIN1 in DM muscle cells. By deciphering the mechanism of BIN1 splicing mis-regulation we demonstrate that the splicing regulator, MBNL1, which is sequestered by expanded CUG and CCUG in DM, binds the BIN1 pre-mRNA and regulates directly its alternative splicing. Finally, reproducing BIN1 splicing alteration in mice is sufficient to reproduce the DM features of T-tubule alterations and muscle weakness. We propose that alteration of BIN1 alternative splicing regulation leads to muscle weakness, a predominant pathological feature of DM. Exon-Array analysis of control and CDM1 muscle primary cultures 10 days of differentiation

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