Similar Datasets
Project description:Deletion of AMPK significantly extended the onset of leukemogenesis and depleted leukemia initiating cells (LICs). To identify how AMPK regulates LICs, we performed gene expression profiling of LICs isolated from AMPK wild type leukemic mice or AMPK-deficient leukemic mice. 4 groups were analyzed; 1) Whole leukemia (GFP+) from AMPK WT ( AMPKfl/fl) mice, 2) Whole leukemia (GFP+) from AMPK-deficient ( AMPK?/?l) mice, 3) LICs=L-GMP (GFP+,lin-,c-kit+, CD16/32+,CD34+) cells from AMPK WT ( AMPKfl/fl) mice, 4) LICs=L-GMP (GFP+,lin-,c-kit+, CD16/32+,CD34+) cells from AMPK-deficient ( AMPK?/?l) mice.
2015-01-01 | E-GEOD-64602 | biostudies-arrayexpress
Project description:Purpose: Next-generation sequencing (NGS) to reveal CIC target genes in CD4 T cells. The goals of this study are to compare NGS-derived CD4 T cell transcriptome in the presence or absence of CIC.
2017-05-22 | GSE84125 | GEO
Project description:The purpose of this study is to compare transcriptional profiles of WT and STAT4-deficient Th17 cultured cells from mice with experimental autoimmune encephalomyelitis (EAE) using RNA sequencing. WT and STAT4 deficient splenocytes from EAE immunized mice were cultured with MOG peptide under Th17 conditions for three days, and then total RNA was extracted from CD4 T cells for sequencing. Differential gene expression was determined using the DESeq2 algorithm. These data reveal a previously unrecognized role for STAT4 in Th17 gene expression and function.
2023-03-30 | GSE227049 | GEO
Project description:The metabolic kinase AMPK regulates transcription in response to nutrient status. AMPK is highly phosphorylated at position Ser184 in the regulatory beta2-subunit, however it's function is unknown. Our preliminary data indicate AMPK dephosphorylated at beta2-Ser184 has elevated nuclear activity and down-regulates apoptotic pathways in response to environmental insult. Here we compare transcriptomes of HEK293T cells expressing either endogenous level beta2 WT or the non-phosphorylatable mutant beta2-Ser182Ala, to gain insight into functional effects of elevated nuclear AMPK activity
2025-02-27 | GSE272077 | GEO
Project description:Purpose: We compared the transcriptomes of murine CD4 T cells lacking either the vhl gene ( vhlfl/fl cd4 cre (vhl cKO) ) or both vhl and hif1a (hif1afl/fl vhlfl/fl cd4 cre (dcKO)) with WT controls before and 24 h after T cell receptor stimulation using anti-CD3/CD28. Results: Using an optimized data analysis workflow, about 45-60 million sequence reads per sample to the mouse genome (build mm10) and identified ca 12500 transcripts in the CD4 T cells of WT and mutant mice after performing HISAT2 alignements to the mm10 reference. Conclusion: the segregation of the transcriptome of unstimulated WT CD4 T cells as compared to the other groups. Within the TCR-stimulated groups the gene expression of vhl cKO CD4 T cells differed to that of WT and vhl hif1a dcKO CD4 T cells which showed in comparison important similarity between them
2022-06-01 | GSE190791 | GEO
Project description:To understand how KMT2D impacts anti-viral CD4 T-cell responses, we performed scRNA-seq on WT and KMT2D-/- effector CD4 T-cells obtained from LCMV Armstrong infected mice
2025-05-09 | GSE282033 | GEO
Project description:5’-AMP-Activated Protein Kinase (Ampk) is an energy gatekeeper that responds to decreases in available ATP by inhibiting energy-consuming processes like protein synthesis and promoting energy-generating processes like glucose uptake. Recently, our lab showed that Lkb1, a previously unstudied kinase in B cell immunology and the main upstream kinase of Ampk, had a critical and unexpected role in B cell activation and germinal center formation. In T cells knockout of the downstream target Ampk, only partially phenocopies Lkb1 deletion, so we sought to determine whether the role of Lkb1 in B cells depends on Ampk. We find Ampk is activated upon B cell stimulation in vitro. Surprisingly, however, Ampk activation occurs in the absence of energetic stress, and B cells continue to grow and divide despite Ampk activity. We performed an IP-MS substrate screen to identify Ampk targets and only identified a limited repertoire of canonical targets, and many non-canonical targets. Despite activation of Ampk and the major role of Lkb1 in B cell activation, B cell specific deletion of Ampk does not significantly affect B cell activation, differentiation, carbon handling, gene expression, or humoral immune responses. The only major effect of Ampk loss was accelerated downregulation of IgD during stimulation, which was preceded by downregulation of the IgD regulator Zfp318. Early activation of Ampk by pharmacological means also has little impact on B cell function, although treatment with the biguanide Phenformin critically impairs germinal center formation and class switch recombination in vivo, but does not significantly impair antigen-specific antibody responses. Combined, our results suggest an unexpected and unexplained activation of Ampk in B cells.
2019-06-16 | GSE121025 | GEO
Project description:Purpose: The aim of this study is compare the gene expression profiles between wild-type (WT) and Etv5-deficient follicular helper T (TFH) cells to identify the molecular mechanism of how ETV5 promotes the TFH cell differentiation. Methods: TFH cells (CD4+CD44+CXCR5+PD-1+) from the spleen of WT and Etv5f/f;Cd4-Cre mice immunized with OVA in alum for 7 days were sorted by a MoFlo-XDP (Beckman Coulter). Total RNA was extracted using TRIzol (GeneAll) according to the manufacturer’s instruction. The library for RNA sequencing was generated using the Truseq stranded mRNA library prep kit (Illumina), and sequencing was performed with Novaseq 6000 (Illumina). Results: Reads were mapped to the mouse reference genome (mm10) with Tophat (v2.0.13), and the aligned results were analyzed with Cuffdiff (v2.2.0) for differentially expressed genes (DEGs). A total of 92 genes were differentially expressed in Etv5-deficient TFH cells (46 genes upregulated and 46 genes downregulated) when compare with WT TFH cells (fold change > 2 and P-value < 0.05). Conclusions: Our study presents the first comparative gene expression analysis of TFH cells from control and T cell-specific Etv5-deficient mice. Since ETV5 usually acts as a transcription activator, we focused on the downregulated genes in Etv5-deficient TFH cells. Through this study, we identified the candidate genes that are targeted by ETV5 for TFH cell differentiation.
2023-11-08 | GSE247030 | GEO
Project description:Purpose: We compared the transcriptomes of mouse CD4 T cells lacking the vhl gene ( vhlfl/fl cd4 cre= vhl cKO) with WT controls from the lungs of mice 8 weeks after aerosol infection with Mycobacterium tuberculosis. Results: Using an optimized data analysis workflow, between 40-55 million sequence reads per sample to the mouse genome (build mm10) and identified 14700 transcripts in the CD4 T cells of WT and mutant mice after performing HISAT2 alignements to the mm10 reference. Conclusion: The transcriptome of WT anf vhl cKO was compared. Groups did cluster differentially with regards to their transcript abundance. The WT group has enriched DNA synthesis/ proliferation pathways whereas the Vhl cKO was enriched in hypoxia pathways. Transcripts assocaited with T cell differentiation were increased in WT group while T cell inhibitory molecules was elevated in the transcriptome of vhl cKO CD4 T cells.
2022-06-01 | GSE190909 | GEO
Project description:Purpose : The goal of this study is to compare the repertoire of T cell receptor (TCR) alpha and beta chain between WT and CIC-deficient thymic CD4+ single positive (SP) T cells, in both non-Treg and Treg populations, to confirm the effect of CIC deficiency on T cell development in the aspect of TCR repertoire. Methods : Treg (CD4+CD8-CD25+GFP+) and non-Treg (CD4+CD8-GFP-) cells from Foxp3-GFP;Cicf/f and Foxp3-GFP;Cicf/f;Vav1-Cre mice were sorted by MoFlo-XDP (Beckman Coulter). Total RNA was extracted using RiboEX (GeneAll) according to the manufacturer's instructions. RNA was then amplified using a commercially available multiplex primer mix covering the TCR alpha and beta chains in two separate PCR reactions. Reverse transcription and subsequent PCR amplification (RT-PCR1) were performed using the Qiagen OneStep RT PCR mix (Qiagen). The cDNA was selected and unused primers were removed by SPRIselect bead selection (Beckman Coulter) followed by a second round of amplification performed with a pair of primers specific for communal sites engineered onto the 5ʹ end of the C- and V- primers used during RT-PCR1. After library preparation, paired-end sequencing was performed using the Illumina Miseq v3 600-cycle Reagent Kit (Illumina). Results : We observed increased frequency of TCRs with long CDR3 length in CIC-deficient non-Treg and Treg cells. We also found significant alterations in the TCR repertoire of TCR beta chain in CIC-deficient Treg cells compared to WT cells, including altered frequency of V and J chain usage. Conclusions : Our study represents the first comparative analysis of TCR repertoire of thymic CD4 SP cells from WT and hematopoietic lineage cell-specific Cic deficient mice. We concluded that CIC deficiency leads to alterations in TCR repertoire of thymic Treg cells.
2021-05-07 | GSE173996 | GEO