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Next Generation Sequencing of WT, ORP4L KI, Wild-type, LCK/R26Tax, ORP4Lcko LCK/R26Tax T-cells Transcriptomes.

ABSTRACT: Next Generation Sequencing of WT, ORP4L KI, Wild-type, LCK/R26Tax, ORP4Lcko LCK/R26Tax T-cells Transcriptomes.

PROVIDER: PRJNA680501 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13125343_1.fastq.gz	Fastqsanger.gz
	SRR13125343_2.fastq.gz	Fastqsanger.gz
	SRR13125344_1.fastq.gz	Fastqsanger.gz
	SRR13125344_2.fastq.gz	Fastqsanger.gz
	SRR13125345_1.fastq.gz	Fastqsanger.gz

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Project description:Purpose: The goals of this study is to uncover the cellular pathways that are essential for T-cell malignant transformation driven by ORP4L and HTLV-1 oncogene Tax. Methods: T-cell mRNA profiles of WT, ORP4L KI, Wild-type, LCK/R26Tax, ORP4Lcko;LCK/R26Tax mice were generated by deep sequencing, using Illumina NovaSeq 6000 sequencer for 318 cycles.Reads that passed the Illumina quality filters were kept for the subsequent analyses. Adapters were trimmed from the reads, and reads shorter than 17 nt were discarded. The reads were mapped to the Mouse mRNA reference database using FANSe3 algorithm on Chi-Cloud NGS Analysis Platform (Chi-Biotech Co. Ltd., Shenzhen, China). Results: We use edgeR to analysis ORP4kI-vs-WT, LCK/R26Tax-vs-Wild-type，ORP4Lcko;LCK/R26Tax-vs-Wild-type，with a |log2 (FoldChange)| > 1 and p value <0.01. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to promote T-cell malignant. Conclusions: Our study represents the first detailed analysis of transcriptomes that promote T-cell malignant transformation driven by HTVL-1 oncogene Tax.

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