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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE162074 | GEO | 2023/11/11

REPOSITORIES: GEO

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Next Generation Sequencing of transcriptomes in GFP+-HSCs sorted from bone marrow of mice receiving HSCs subjected to control RNA or miR-31-5p inhibitor treatment.

Project description:Purpose: The goals of this study is to uncover the difference of transcriptomes that are essential for HSCs malignant transformation driven by miR-31-5p inhibition. Methods: GFP+-HSCs sorted from bone marrow mRNA profiles of mice receiving HSCs subjected to control RNA or miR-31-5p inhibitor treatment 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 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 HSCs malignant driven by miR-31-5p inhibition. Conclusions: Our study represents the first detailed analysis of transcriptomes that promote T-cell malignant transformation driven by HTVL-1 oncogene Tax.

2023-12-29 | GSE163985 | GEO

Next Generation Sequencing of wild-type and ORP4L knock-in murine T-cells Transcriptomes

Project description:Purpose: The goals of this study is to determine whether specific gene sets are dysregulated in the murine ORP4L knock-in T-cells, as compared to wild-type T-cells. Methods: T-cell mRNA profiles of wild-type and ORP4L knock-in 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 Plantform. Results: We use edgeR to analysis ORP4 kncok-in vs. wild-type，with a |log2 (FoldChange)| > 1 and p value <0.01. Hierarchical clustering of differentially expressed genes uncovered a total of 970 differentially expressed genes (DEGs) , of which 539 were down-regulated and 431 up-regulatedseveral. Conclusions: Our study represents the first detailed analysis of transcriptomes that promote T-cell malignant transformation driven by oncogene ORP4L in mice.

2022-06-04 | GSE199958 | GEO

Expression data from Lck-Dlx5 lymphoma

Project description:Lck-Dlx5 induces T-cell lymphoma but the mechanism is unknown. We used microarrays to detail the global programme of gene expression underlying Dlx5-induced T-cell lymphoma T-cells were isolated from Lck-Dlx5 mice, Lck-MyrAkt2 mice and Wild type littermates for RNA extraction and hybridization on Affymetrix microarrays.

2016-06-24 | E-GEOD-83685 | biostudies-arrayexpress

RNA Expression Data from IL-15-/- and IL-15+/+ TAX-LUC Mouse Tumors

Project description:IL-15 is recognized as a promising candidate for tumor immunotherapy and has been described as both a promoter of cancer and a promoter of anti-cancer immunity. IL-15 was discovered in cells transformed by HTLV-1, the etiologic agent of adult T cell leukemia / lymphoma (ATL) and the human retrovirus that carries the Tax oncogene. We have developed the TAX-LUC mouse model of ATL in which Tax expression drives both malignant transformation and luciferase expression, enabling non-invasive imaging of tumorigenesis in real time. To identify the role of IL-15 in spontaneous development of lymphoma in vivo, an IL-15-/- TAX-LUC strain was developed and examined. The absence of IL-15 resulted in aggressive tumor growth and accelerated mortality and demonstrated that IL-15 was not required for Tax-mediated lymphoma but was essential for anti-tumor immunity. Further analysis revealed a unique transcriptional profile in tumor cells that arise in the absence of IL-15 that included a significant increase in the expression of IL-1α and IL-1α-regulated cytokines. Moreover, anti-IL-1α antibodies and an IL-1 receptor antagonist (Anakinra) were used to interrogate the potential of IL-1α targeted therapies in this model. Taken together, these findings identify IL-15 and IL-1α as therapeutic targets in lymphoma. We used microarrays to compare the gene expression profile of tumors in IL-15-/- TAX-LUC mice to IL-15+/+ TAX-LUC mice RNA was obtained from CD16/32HI and CD16/32LO cells harvested from n=2 IL-15+/+ (control)and n=2 IL-15-/- Tax tumors and was compared to look for alterations in gene expression in malignant and tumor infiltrating cells resulting from loss of IL-15 in vivo

2013-06-11 | E-GEOD-46072 | biostudies-arrayexpress

Lck phosphorylation status of Lck Tyr192 and Tyr192/Tyr505 mutantsLck phosphorylation status of Lck Tyr192 and Tyr192/Tyr505 mutants

Project description:Lymphocyte-specific protein tyrosine kinase (Lck) is crucial for signaling from the T cell receptor (TCR) and is controlled through tyrosine phosphorylations. Phosphorylated Tyr505 (pTyr505) promotes a closed, inactive conformation of Lck, while pTyr394 is critical for kinase activity. Additionally, pTyr192 has been suggested to regulate Lck activity by changing the specificity of the Lck Src-homology 2 (SH2) domain and/or by affecting Lck association with CD45 thus drastically increasing pTyr505. However, little is known about how pTyr192 affects endogenously expressed Lck. Here we used CRISPR/Cas9 genome editing to generate Jurkat cell lines expressing Lck Glu192 mimicking Lck pTyr192, or Lck Phe192 mimicking unphosphorylated Lck Tyr192. We confirmed that Lck Glu192 is hyperphosphorylated on Tyr505, possibly explaining reduced association of Lck Glu192 with prototypic Lck-SH2 ligands. To isolate the effect of Lck Tyr192 mutations from the effect on Lck pTyr505, we subsequently generated Jurkat cells doubly mutated on Lck Tyr192 and Lck Tyr505. Both Lck Phe192/Phe505 and Lck Glu192/Phe505 mutants co-precipitated similar amounts of binding partners. Moreover, both mutants displayed hyperphosphorylation of Tyr394. Our results indicate that CD45 is the main phosphatase controlling Lck pTyr394 in steady-state T cells. Additionally, our data demonstrate that the prototypic specificity of the Lck SH2 domain (owned by the Lck Phe192 mutants) promotes transphosphorylation of Tyr394. These observations pinpoint the fundamental role of Tyr192 in regulation of Lck activity and simultaneously reveal the most potent Lck mutants so far described

2021-04-02 | PXD014470 | Pride

RNA Expression Data from IL-15-/- and IL-15+/+ TAX-LUC Mouse Tumors

2013-06-11 | GSE46072 | GEO

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2021-01-05 | GSE158457 | GEO

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2015-09-15 | E-MTAB-3242 | biostudies-arrayexpress

Quantitative interactomics of Lck-TurboID in living human T cells unveils T cell receptor stimulation-induced proximal Lck interactors

Project description:While Lck has been widely recognized to play a pivotal role in the initiation of the T cell receptor (TCR) signaling pathway, an understanding of the precise regulation of Lck in T cells upon TCR activation remains elusive. Investigation of protein-protein interaction (PPI) using proximity labeling techniques such as TurboID has the potential to provide valuable molecular insights into Lck regulatory networks. By expressing Lck-TurboID in Jurkat T cells, we have uncovered a dynamic, short-range Lck protein interaction network upon 30 minutes of TCR stimulation. In this novel application of TurboID, we detected 27 TCR stimulation-induced Lck-proximal interactors in living T cells, including both bona fide and uncanonical Lck interactors, validating the discovery power of this tool. Our results revealed previously unappreciated Lck PPI which may be associated with cytoskeletal rearrangement, ubiquitination of TCR signaling proteins, activation of the MAPK cascade, coalescence of the LAT signalosome, and formation of the immunological synapse. In this study, we demonstrated for the first time in immune cells and for the kinase Lck that TurboID can be utilized to unveil PPI dynamics in living cells at a time scale consistent with TCR signaling.

2020-11-12 | PXD020759 | Pride

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