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RAN-seq analysis comparing gene expression difference between control and Decr2 knock-down B16.SIY tumors

ABSTRACT: RAN-seq analysis comparing gene expression difference between control and Decr2 knock-down B16.SIY tumors

PROVIDER: PRJNA803438 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17883886.fastq.gz	Fastqsanger.gz
	SRR17883887.fastq.gz	Fastqsanger.gz
	SRR17883888.fastq.gz	Fastqsanger.gz
	SRR17883889.fastq.gz	Fastqsanger.gz
	SRR17883890.fastq.gz	Fastqsanger.gz

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RAN-seq analysis comparing gene expression difference between control and Decr2 knock-down B16.SIY tumors

Project description:Purpose: To undstand the mechanism by which Decr2 knock-down tumors were resistant to CD8+ T cell killing in vitro and anti-PD-L1 therapy in vivo, we performed RNA-seq analysis comparing Decr2-knockdown versus control B16.SIY cells Methods: mRNA was isolated from Decr2 shRNAs (2 shRNA) and Control shRNA infected B16.SIY cells. mRNA profiles were generated by deep sequencing, in triplicate, using the Illumina HiSeq platform. Alignment was performed using the Kallisto software. All submitted samples passed quality control using the R package FastQC. Raw read counts were processed by TMM normalization followed by log2 transformation. Limma voom was used to identify differentially expressed genes between DECR2 knockdown and control cells.

2022-02-11 | GSE196123 | GEO

RNA-seq analysis of dark-induced senescence of the leaves of Ran-GDP and Ran-GTP overexpression transgenic plants

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Lack of RAN-mediated toxicity in Huntington’s disease knock-in mice

Project description:Identification of repeat-associated non-AUG (RAN) translation in trinucleotide (CAG) repeat diseases leads to an emerging concept that CAG repeat diseases are caused by non-polyglutamine products. Nonetheless, the exact contribution of RAN translation to the pathogenesis of CAG repeat diseases remains elusive. Via CRISPR/Cas9-mediated genome editing, we established new knock-in mouse models that harbor expanded CAG repeats in the mouse huntingtin gene, which express RAN translated products or polyglutamine products respectively. Here we report that RAN translation is not detected in the knock-in mouse models, and that only the expanded polyglutamine products can cause neuropathology and behavioral phenotypes. Therefore, polyglutamine products, rather than RAN translated products, play a major role in the pathogenesis of CAG repeat diseases.

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Project description:Whole Genome Sequencing of the murine breast cancer cell line 4T1 and of the murine melanoma cell line B16-ova was carried out with the aim of identifying somatic mutations. We also ran deep Mass Spectrometry proteomics analysis on the same cell lines, aiming to determine which somatic mutations carry over to the protein expression level. Further, we tested these cancer specific protein epitopes (putative neoantigens) for immunogenicity using mouse models. Finally, the putative neoantigens that showed good immunogenic potential were used in tumor growth control experiments with mice engrafted with the two tumor cell lines. In these experiments we tested whether cancer vaccines based on individual neoantigen peptides (MHC-I) restricted the growth of the tumor compared to adequate controls. The overall aim of the project is to validate the ability of our multi-omics/bioinformatics pipeline to identify and deliver neoantigens that can be used to suppress tumor growth. File names Sample names P10859_101_S1_L001_R1_001_BHKWV3CCXY 4T1_S1_L001_R1_001_BHKWV3CCXY P10859_101_S1_L001_R2_001_BHKWV3CCXY 4T1_S1_L001_R2_001_BHKWV3CCXY P10859_101_S1_L002_R1_001_BHKWV3CCXY 4T1_S1_L002_R1_001_BHKWV3CCXY P10859_101_S1_L002_R2_001_BHKWV3CCXY 4T1_S1_L002_R2_001_BHKWV3CCXY P10859_102_S2_L003_R1_001_BHKWV3CCXY B16-OVA_S2_L003_R1_001_BHKWV3CCXY P10859_102_S2_L003_R2_001_BHKWV3CCXY B16-OVA_S2_L003_R2_001_BHKWV3CCXY P10859_102_S2_L004_R1_001_BHKWV3CCXY B16-OVA_S2_L004_R1_001_BHKWV3CCXY P10859_102_S2_L004_R2_001_BHKWV3CCXY B16-OVA_S2_L004_R2_001_BHKWV3CCXY

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RAN directly binds and stabilizes G3BP1 mRNA in the nucleus to facilitate proliferation and metastasis of nasopharyngeal carcinoma (anti-RAN RIP-seq)

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