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GSE140448
Mus musculus
40 Downloadable Samples
Illumina HiSeq 2000, Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Critical role for TRIM28 and HP1β/γ in the epigenetic control of T cell metabolic reprograming and effector differentiation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 36 Downloadable Samples
Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
Critical role for TRIM28 and HP1b/g in the epigenetic control of T cell metabolic reprogramming and effector differentiation
Publication Title
Critical role for TRIM28 and HP1β/γ in the epigenetic control of T cell metabolic reprograming and effector differentiation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
Critical role for TRIM28 and HP1b/g in the epigenetic control of T cell metabolic reprogramming and effector differentiation
Publication Title
Critical role for TRIM28 and HP1β/γ in the epigenetic control of T cell metabolic reprograming and effector differentiation.
Sample Metadata Fields
Specimen part
View Samples- Drosophila melanogaster
- 64 Downloadable Samples
Illumina HiSeq 4000
Description
To identify genes that mediate altered communication between fat body and peripheral tissues, we report the gene expression changes in Drosophila third instar larval fat bodies with or without constitutively-active Toll (Toll10b) to activate innate immune signaling, myristoylated Akt (myrAkt) to activate insulin signaling, or both transgenes to bypass the block from Toll signaling to the upstream part of the insulin signaling pathway Overall design: Comparison of RFP/GFP (Control), Toll10b/GFP (Toll10b), RFP/myrAkt (myrAkt), and Toll10b/myrAkt (Toll10b + myrAkt)
Publication Title
The Toll Signaling Pathway Targets the Insulin-like Peptide Dilp6 to Inhibit Growth in Drosophila.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 86 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Microarray is widely used to monitor gene expression changes in breast cancer. The transcriptomic changes in breast cancer is commonly occured during the transition of normal cells to cancerous cells. This is the first study on gene expression profiling of multi ethnic of Malaysian breast cancer patients (Malays, Chinese and Indian). We aim to identify differentially expressed genes between tumors and normal tissues. We have identified a set of 33 significant differentially expressed genes in the tumor vs. normal group at p<0.001.
Publication Title
Gene expression patterns distinguish breast carcinomas from normal breast tissues: the Malaysian context.
Sample Metadata Fields
Specimen part, Disease stage, Race
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Hepatocellular carcinoma (HCC) is a highly prevalent and deadly disease world-wide. The survival of HCC patients is usually very poor due to the lack of efficient anti-cancer drugs
Publication Title
Synthesis and bio-molecular study of (+)-N-Acetyl-α-amino acid dehydroabietylamine derivative for the selective therapy of hepatocellular carcinoma.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 21 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
The full complement of molecular pathways contributing to Parkinsons disease (PD) pathogenesis remains unknown. Here, to address this issue, we began by using a high-resolution variant of functional magnetic resonance imaging (fMRI) to pinpoint brainstem regions differentially affected by, and resistant to, the disease. Then, relying on the imaging information as a guide, we profiled gene expression levels of postmortem brain samples and used a factorial statistical model to identify a disease related decrease in the expression of the polyamine enzyme spermidine/spermine N1-acetyltransferase 1 (SAT1). Next, a series of studies were performed to confirm the pathogenic relevance of this finding. First, to test for a causal link between polyamines and -synuclein toxicity, we investigated a yeast model expressing -synuclein. Polyamines were found to enhance the toxicity of -synuclein, and an unbiased genome-wide screen for modifiers of -synuclein toxicity identified Tpo4, a member of a family of proteins responsible for polyamine transport. Second, to test for a causal link between SAT1 activity and PD histopathology we investigated a mouse model expressing -synuclein. DENSPM (N1, N11-diethylnorspermine), a polyamine analog that increases SAT1 activity, was found to reduce PD histopathology, while Berenil (diminazene aceturate), a pharmacological agent that reduces SAT1 activity, worsened the histopathology. Third, we genotyped PD patients and controls and isolated a rare but novel variant in the SAT1 gene, although the functional significance of this genetic variant was not identified. Taken together, the results suggest that the polyamine pathway contributes to PD pathogenesis.
Publication Title
Polyamine pathway contributes to the pathogenesis of Parkinson disease.
Sample Metadata Fields
Sex, Age, Subject
View Samples- Mus musculus
- 21 Downloadable Samples
- NextSeq 500, Illumina HiSeq 2000
Description
Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Decreased expression of C9orf72 is seen in expansion carriers, suggesting loss of function may play a role in disease. We find that two independent mouse lines lacking the C9orf72 ortholog (3110043O21Rik) in all tissues developed normally and aged without motor neuron disease. Instead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of engorged macrophage-like cells. C9orf72 expression was highest in myeloid cells, and loss of C9orf72 led to lysosomal accumulation and altered immune responses in macrophages and microglia, with age-related neuroinflammation similar to C9orf72 ALS but not sporadic ALS patient tissue. Thus, C9orf72 is required for normal function of myeloid cells, and altered microglial function may contribute to neurodegeneration in C9orf72 expansion carriers. Overall design: To compare the RNA Seq profiles from the lumbar region of spinal cords from mice lacking one copy or both copies of the C9orf72 ortholog (3110043O21Rik) compared to wild type control with two copies at 3 months (n=3) and 17 months (n=4).
Publication Title
C9orf72 is required for proper macrophage and microglial function in mice.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
- IlluminaHiSeq2000
Description
Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative condition characterized by loss of motor neurons in the brain and spinal cord. Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9ORF72 gene are the most common cause of the familial form of ALS (C9-ALS), as well as frontotemporal lobar degeneration and other neurological diseases. How the repeat expansion causes disease remains unclear, with both loss of function (haploinsufficiency) and gain of function (either toxic RNA or protein products) proposed. We report a cellular model of C9-ALS with motor neurons differentiated from induced pluripotent stem cells (iPSCs) derived from ALS patients carrying the C9ORF72 repeat expansion. No significant loss of C9ORF72 expression was observed, and knockdown of the transcript was not toxic to cultured human motor neurons. Transcription of the repeat was increased, leading to accumulation of GGGGCC repeat–containing RNA foci selectively in C9-ALS iPSC-derived motor neurons. Repeat-containing RNA foci colocalized with hnRNPA1 and Pur-a, suggesting that they may be able to alter RNA metabolism. C9-ALS motor neurons showed altered expression of genes involved in membrane excitability including DPP6, and demonstrated a diminished capacity to fire continuous spikes upon depolarization compared to control motor neurons. Antisense oligonucleotides targeting the C9ORF72 transcript suppressed RNA foci formation and reversed gene expression alterations in C9-ALS motor neurons. These data show that patient-derived motor neurons can be used to delineate pathogenic events in ALS. Overall design: Transcriptome profiling from iPSC derived motor neurons compared to controls
Publication Title
Targeting RNA foci in iPSC-derived motor neurons from ALS patients with a C9ORF72 repeat expansion.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 23 Downloadable Samples
- Illumina HiSeq 2000, Ion Torrent Proton
Description
Noncoding expansions of a hexanucleotide repeat (GGGGCC) in the C9orf72 gene are the most common cause of familial amyotrophic lateral sclerosis and frontotemporal dementia. Here we report transgenic mice carrying a bacterial artificial chromosome (BAC) containing the full human C9orf72 gene with either a normal allele (15 repeats) or disease-associated expansion (~100–1,000 repeats; C9-BACexp). C9-BACexp mice displayed pathologic features seen in C9orf72 expansion patients, including widespread RNA foci and repeat-associated non-ATG (RAN) translated dipeptides, which were suppressed by antisense oligonucleotides targeting human C9orf72. Nucleolin distribution was altered, supporting that either C9orf72 transcripts or RAN dipeptides promote nucleolar dysfunction. Despite early and widespread production of RNA foci and RAN dipeptides in C9-BACexp mice, behavioral abnormalities and neurodegeneration were not observed even at advanced ages, supporting the hypothesis that RNA foci and RAN dipeptides occur presymptomatically and are not sufficient to drive neurodegeneration in mice at levels seen in patients. Overall design: To compare the RNA Seq profiles from the cortex and spinal cord of transgenic mice expressing unexpanded human C9orf72 (F08, n=4), expanded human C9orf72 (F112, n=3/4), and nontransgenic controls (n=4).
Publication Title
C9orf72 BAC Transgenic Mice Display Typical Pathologic Features of ALS/FTD.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples