Gene expression difference between normal and Pten-deficient 5-HT neurons
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ABSTRACT:
PROVIDER: PRJNA691327 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13404673.fastq.gz | Fastqsanger.gz | |||
| SRR13404673_1.fastq.gz | Fastqsanger.gz | |||
| SRR13404673_2.fastq.gz | Fastqsanger.gz | |||
| SRR13404674.fastq.gz | Fastqsanger.gz | |||
| SRR13404674_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: compare the gene expression diffenrence between wildtype and Pten-deficient 5-HT neurons. Methods: 5-HT neurons cell body are collected from acut brain slice with patch electrodes. Pten-deficient 5-HT neurons are obtained from Pet1-Cre; Ptenflox/flox mice. Normal 5-HT neurons are obtained from littermate wildtype mice. Reverse transcription was performed using a SMARTer Ultra Low RNA Kit (Clontech, Japan). Single-cell cDNA was amplified using an Advantage 2 PCR Kit (Clontech, Japan). Purified cDNA from individual cells were sequenced using the Illumina HiSeq 2000 platform. Sequence reads were aligned to the mouse mm9 genome using TopHat. Differential expression analysis was performed using DESeq (Bioconductor) followed by Student t-test. Genes were considered differentially expressed if p<0.05. Results: The somatic compartments of individual YFP-labeled 5-HT neurons in acute brain slices were harvested for RNA sequencing. Each of the cells had 2 X 107 reads mapping back to the mouse genome when analyzed using the RUM mapping program. We found 859 genes (381 up-regulated, 478 down-regulated) were differentially expressed in Pten-deficient 5-HT neurons. Gene ontology of differentially expressed genes revealed the biological processes up-regulated and down-regulated in Pten-deficient 5-HT neurons. The absence of Pten in 5-HT neurons was associated with significantly increased expression of genes involved in the regulation of axonal extension and cell size, cell morphogenesis and cytoskeleton organization
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Project description:Transcriptome comparisons by RNAseq of genetically engineered mouse models of synovial sarcoma, expressing SS18-SSX1 or SS18-SSX2 and having homozygous conditional genetic silencing of Pten or wildtype Pten.
2016-11-03 | GSE81476 | GEO
Project description:PTEN is a tumor suppressor that is often inactivated in cancer and possesses both lipid and protein phosphatase activities. We report the metabolic regulator PDHK1 (pyruvate dehydrogenase kinase1) is a synthetic-essential gene in PTEN-deficient cancer and normal cells. The predominant mechanism of PDHK1 regulation and dependency is the PTEN protein phosphatase dephosphorylates NFkB activating protein (NKAP) and limits NFkB activation to suppress expression of PDHK1, a NFkB target gene. Loss of the PTEN protein phosphatase upregulates PDHK1 to drive aerobic glycolysis and induce PDHK1 cellular dependence. PTEN-deficient human tumors harbor increased PDHK1, which is a biomarker of decreased patient survival, establishing clinical relevance. This study uncovers a PTEN-regulated signaling pathway and reveals PDHK1 as a potential target in PTEN-deficient cancers.
2019-09-09 | PXD014707 | Pride
Project description:Experiment: Establishment of expression profiles in HT, PTC with HT, PTC without HT, and mPTC in comparison to TN samples. TN samples were downloaded as CEL files from the repository of the microarray vendor. Biostatistical analysis focussed in first instance on identifying genes and biofunctions related to HT and PTC with HT.
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Project description:Mice with (i) PR-Cre; (ii) PR-Cre, Fbxw7 R482Q/+; (iii) PR-Cre, Pten fl/fl; (iv) PR-Cre, Pten fl/fl, Fbxw7 R482Q/+ Uterine RNA was harvested at 8 weeks age and expression profiling done by Affymetrix Clariom S Mouse HT array
2023-07-01 | GSE232356 | GEO
Project description:To investigate the gene expression difference in peri-infarct neurons of Padi4-deficient and control mice on day 4 after ischemic stroke onset, we performed gene expression profiling analysis using data obtained from RNA-seq of peri-infarct neurons from neuron-specific Padi4-deficient and control mice.
2023-07-24 | GSE232429 | GEO
Project description:Intestinal polyposis, a precancerous neoplasia, results primarily from an abnormal increase in the number of crypts. Crypts contain intestinal stem cells (ISCs). Thus intestinal polyposis provides an ideal condition for studying stem cell involvement in polyp/tumor formation. Using a conditional knock-out mouse model, we found that the tumor suppressor Phosphatase of Tension homolog (PTEN) governs the proliferation rate and number of ISCs and loss of PTEN results in an excess of ISCs. In PTEN mutants, excess ISCs initiate de-novo crypt formation and crypt fission, recapitulating crypt production in fetal/neonatal intestine. Microarray studies were used to profile the changes in gene expression that occurred when PTEN was knocked out in the intestine. Keywords: Disease state analysis, genetic modification, Intestinal polyposis, PTEN mutant, Cowden disease mouse model
2006-11-18 | GSE6078 | GEO
Project description:Loss of the PTEN tumor suppressor is one of the most common oncogenic drivers across all cancer types. PTEN is the major negative regulator of phosphoinositide-3 kinase (PI3K) signaling. Notably, the PI3Kβ isoform has been shown to play an important role in PTEN-deficient tumors, but the mechanisms underlying the importance of PI3Kβ activity remain elusive. Using a syngeneic genetically-engineered mouse (GEM) model of invasive breast cancer driven by concurrent ablation of Pten and Trp53 (p53), we showed that genetic inactivation of PI3Kβ led to a robust anti-tumor immune response that abrogated tumor growth in syngeneic immunocompetent mice, but not in immunodeficient mice. Mechanistically, PI3Kβ inactivation in the PTEN-null setting led to reduced STAT3 signaling and increased expression of immune stimulatory molecules, thereby promoting anti-tumor immune responses. Pharmacological PI3Kβ inhibition also elicited anti-tumor immunity, and synergized with immunotherapy to inhibit tumor growth. Mice with complete responses to the combined treatment displayed immune memory and rejected tumors upon re-challenge. Our findings demonstrate a molecular mechanism linking PTEN loss and STAT3 activation in cancer and suggest that PI3Kβ controls immune escape in PTEN-null tumors, providing a rationale for combining PI3Kβ inhibitors with immunotherapy for the treatment of PTEN-deficient breast cancer.
2023-03-07 | GSE225064 | GEO
Project description:Glioblastoma (GBM) is a highly lethal brain tumor presenting as one of two subtypes with distinct clinical histories and molecular profiles. The primary GBM subtype presents acutely as high-grade disease that typically harbors EGFR, PTEN and Ink4a/Arf mutations, and the secondary GBM subtype evolves from the slow progression of low-grade disease that classically possesses PDGF and p53 events1. Here, we show that concomitant CNS-specific deletion of p53 and Pten in the mouse CNS generates a penetrant acute-onset high-grade malignant glioma phenotype with striking clinical, pathological and molecular resemblance to primary GBM in humans. This genetic observation prompted p53 and PTEN mutational analysis in human primary GBM, demonstrating unexpectedly frequent inactivating mutations of p53 as well the expected PTEN mutations. Integrated transcriptomic profling, in silico promoter analysis and functional studies of murine neural stem cells (NSCs) established that dual, but not singular, inactivation of p53 and Pten promotes an undifferentiated state with high renewal potential and drives elevated c-Myc levels and its associated signature. Functional studies validated increased c-Myc activity as a potent contributor to the impaired differentiation and enhanced renewal of p53-Pten null NSCs as well as tumor neurospheres (TNSs) derived from this model. c-Myc also serves to maintain robust tumorigenic potential of p53-Pten null TNSs. These murine modeling studies, together with confirmatory transcriptomic/promoter studies in human primary GBM, validate a pathogenetic role of a common tumor suppressor mutation profile in human primary GBM and establish c-Myc as a key target for cooperative actions of p53 and Pten in the regulation of normal and malignant stem/progenitor cell differentiation, self-renewal and tumorigenic potential. We used microarrays to detail the gene expression difference of the p53-null and p53/Pten-doubly null neural stem cell after differentiation . Keywords: cell type comparison
2008-10-01 | GSE12694 | GEO
Project description:T cell-specific deletion of PTEN induces premalignancy in CD4+ CD8+ (DP) immature T cells in the thymus, which progresses to the development of mature CD4+ T cell lymphomas in the lymph nodes and spleen. As part of a screen to identify factors that inhibit progression to malignancy, we compared miRNA expression in premalignant PTEN-deficient DP thymocytes versus wild-type controls. DP thymocytes were collected by cell sorting from three 9-week-old, premalignant T cell-specific PTEN-deficient mice (tPTEN-/-) and three littermate controls. miRNA expression was assessed relative to a reference pool generated from an equal mixture of all samples.
2014-04-12 | E-GEOD-56759 | biostudies-arrayexpress