Expression data from Lck-Dlx5 lymphoma
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: yinfei tan
PROVIDER: E-GEOD-83685 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transcriptome analysis of effect of Lockd knockout on cells Many long non-coding (lnc) RNAs are reported to regulate gene expression and protein functions. However, the proportion of lncRNAs with biological activities among the thousands expressed in mammalian cells is controversial. We studied Lockd (Downstream of p27), a 434 bp polyadenylated lncRNA originating 4 kb 3â to the Cdkn1b gene. Heterozygous and homozygous deletion of the 25 kb Lockd locus reduced Cdkn1b transcription by approximately 35 and 70% respectively in a mouse erythroid cell line. In contrast, homozygous insertion of a polyadenylation cassette 80 bp downstream of the Lockd transcription start site reduced the entire lncRNA transcript level by > 90%, but had no effect on Cdkn1b transcription. The 5â region of the Lockd gene contains a DNase hypersensitive site, binds numerous transcription factors (TFs), and physically associates with the Cdkn1b promoter in chromosomal conformation capture (NG Capture-C) studies. Thus, the Lockd gene positively regulates Cdkn1b transcription through an enhancer-like cis element and not via the lncRNA transcript. These findings demonstrate that the biological functions of a lncRNA cannot be inferred simply from phenotypes that arise after deleting the corresponding genomic locus. We analyzed mouse G1E erythroid cell line clones with Control Lockd (C - 3 replicates) and with Lockd deletion with CRISPR (KO - 4 replicates) using Mouse Gene 2.0 ST Array platform (transcript version). Array data was processed by RMA algorithm.
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Project description:Objective: Microarray analysis was used to determine the molecular mechanism underlying Fancd2 and Foxo3a double knockout mice HSCs exhaustion. Methods: SLAM cells were obtained from WT, Fancd2KO, Foxo3aKO and DKO bone marrow cells. Total RNA from SLAM cells was purified by RNeasy kit (Qiagen) following the manufacturer’s procedure. And then the RNA was fluorescently labeled and hybridized to Affmetrix Mogene 2.0 ST array. Data was analyzed by Genespring GX11 software. Results: a large proportion of differentially expressed genes in dKO HSCs belonged to cell cycle control. Another group of up-regulated genes were those involved in the differentiation of HSCs. Other differentially regulated transcripts included genes known to be involved in oxidative stress response, or to have roles in DNA repair. Conclusion: Cell cycle, DNA repair, DNA binding and hematopoietic lineage differentiation pathways might have been perturbed in HSC exhaustion. Mouse Femurs and tibias from WT, Fancd2KO, Foxo3aKO and DKO mice were flushed to dissociate the BM fraction. The mononuclear cells were isolated by Ficoll (GE Healthcare) gradient centrifugation. Single SLAM (Lin-ckit+Sca-1+CD34-) cells were sorted. RNA was extracted, labelled, and quantified using the Mouse ST-2 microarray.
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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
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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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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