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GSE81154
Mus musculus
6 Downloadable Samples
Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Evaluation of the role of RIP4 in lung adenocarcinoma revealed that RIP4 inhibits STAT3 signaling in vitro and in vivo. Repression of RIP4 enhanced STAT3 signaling activation in KRAS LSL/G12D/wt; p53flox/flox murine tumors. This promoted cancer dedifferentiation through ECM remodeling
Publication Title
RIP4 inhibits STAT3 signaling to sustain lung adenocarcinoma differentiation.
Sample Metadata Fields
Age, Specimen part
View Samples- Rattus norvegicus
- 2 Downloadable Samples
Illumina HiSeq 2000
Description
L-type voltage gated Ca channels play a critical role in E-C coupling in cardiac muscle. alpha1C is associated with beta auxiliary subunits (b1-b4), which regulate cardiac Ca channel gating properties. Here we report a preliminary exploratory study suggesting a novel role of beta4 subunit in heart. We observed that overexpression of beta4 subunit increases the expression of a wide variety of endogenous genes related to antiviral activity. This includes genes in the downstream signalling of RIG-1 pathway such as RIG-1, Irf7 and Ifitm3. The increase expression of these factors may have an antiviral protective role against infection. Overall design: Examination of an overall differential expression by the beta4 subunit
Publication Title
The β<sub>4</sub> subunit of Ca<sub>v</sub>1.2 channels is required for an optimal interferon response in cardiac muscle cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The Transcription Factor Tcf1 Contributes to Normal NK Cell Development and Function by Limiting the Expression of Granzymes.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The transcription factor Tcf1 plays an essential role for the development of NK cells, however, its precise role for NK cell development, maturation and function is poorly understood. Here we show that distinct domains of Tcf1 direct bone marrow progenitors towards the NK cell lineage and mediate lineage commitment and NK cell expansion, and that Tcf1 downregulation is required for terminal NK cell maturation. Impaired NK cell development in the absence of Tcf1 is explained by increased cell death due to excessive expression of Granzyme family proteins, which results in NK cell self-destruction. In addition, excessive Granzyme B expression leads to target cell induced NK cell death and consequently reduced target cell killing by NK cells lacking Tcf1. Mechanistically, Tcf1 prevents excessive Granzyme B expression by binding to a newly identified enhancer element upstream of the Granzyme B locus. These data identify an unexpected requirement to limit the expression of cytotoxic effector molecules for lymphocyte development.
Publication Title
The Transcription Factor Tcf1 Contributes to Normal NK Cell Development and Function by Limiting the Expression of Granzymes.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 51 Downloadable Samples
- Affymetrix Human Gene Expression Array (primeview)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Genomic characterization of liver metastases from colorectal cancer patients.
Sample Metadata Fields
Sex, Age, Disease, Disease stage
View Samples- Mus musculus
- 52 Downloadable Samples
- Illumina HiScanSQ
Description
Background & Aims. Glycine N-methyltransferase (GNMT) is an essential regulator of the total transmethylation flux in the mammalian liver. Distinct DNA methylation patterns are characteristic of liver development, hepatic de-differentiation and liver disease progression, processes in which the levels of GNMT decrease dramatically by mechanisms still poorly understood. Interestingly, putative binding sites for the microRNA miRNA-873-5p were identified in the 3´UTR of GNMT suggesting a potential role for miRNA-873-5p in GNMT regulation. Results. We have identified that the hepatic expression of miRNA-873-5p was increased in a cohort of cirrhotic and liver cancer patients associated with a down-regulation of GNMT levels. Moreover, during liver development, hepatic de-differentiation and fibrosis, the elevation of miRNA-873-5p coincided with the reduction of GNMT expression, indicating that miRNA-873-5p specifically targets the expression of GNMT. Under these circumstances, inhibition of miRNA-873-5p induced GNMT levels and decreased global CpG methylation and transmethylation flux. Indeed, reestablishment of GNMT expression by miRNA-873-5p inhibition reduced hepatocyte de-differentiation, and abolished completely the mortality produced after bile duct ligation as a result of decreased proinflamatory and profibrogenic markers. miRNA-873-5p knockdown-mediated antifibrotic effect was significantly blunted if its effect on GNMT was blocked. Conclusion. Taken together, our studies highlight the role of miRNA-873-5p as a key regulator of GNMT expression, paving the way for new therapeutical approaches in liver de-differentiation and fibrosis. Overall design: Genome-wide changes in gene Expression in mouse livers from BDL treated or not with anti-miR-873 were generated by RNAseq.
Publication Title
MiR-873-5p acts as an epigenetic regulator in early stages of liver fibrosis and cirrhosis.
Sample Metadata Fields
Age, Cell line, Treatment, Subject
View Samples- Mus musculus
- 19 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Metabolomic Identification of Subtypes of Nonalcoholic Steatohepatitis.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 19 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Methionine adenosyltransferase (MAT) enzymes generate SAMe (S-adenosylmethionine), the main biological methyl donor. There are two MAT encoding genes in mammals (Mat1a and Mat2a), which show different activities and cellular distribution. Mat1a encodes the enzyme mainly expressed in normal liver. Mat1a ablation in mice results in the spontaneous development of non-alcoholic steatohepatitis (NASH). We observed that SAMe depletion in Mat1a KO mice had three main effects on hepatic lipid metabolism: 1) impaired TG (triglyceride) export via VLDL; 2) impaired mitochondrial FA (fatty acid) oxidation (as evidenced by membrane depolarization, downregulation of Phb1 (prohibitin 1, a mitochondrial chaperone protein) and Mcj/Dnajc15 (endogenous mitochondrial repressor of respiratory chain), and accumulation of long-chain acylcarnitines); and 3) increased FA uptake. The convergence of these three factors induced TG accumulation in LD (lipid droplets). LD expansion confronts hepatocytes with a high demand of PC (phosphatidylcholine) molecules to cover the LD surface since other phospholipids, such as PE (phosphatidylethanolamine), cannot stabilize LD and prevent coalescence. In Mat1a KO this situation is aggravated, since SAMe-dependent PC synthesis via PE methylation is decreased, the PC/PE ratio reduced and mitochondrial FA oxidation impaired. To put a brake to this drain of PC molecules to LD, FA are rerouted in Mat1a KO mice liver to other catabolic (endoplasmic reticulum and peroxisome oxidation) and biosynthetic (ceramides synthesis) pathways, causing oxidative stress, inflammation and fibrosis. SAMe treatment for two months in 8-9 month old Mat1a KO mice ameliorated mitochondrial dysfunction (reduces membrane depolarization, improves Phb1 and Mcj expression, and increases SAMe transport to mitochondria) improving FA oxidation efficiency (FA and acylcarnitine levels decrease), which results in a drastic reduction in TG accumulation. SAMe treatment in Mat1a KO mice resulted in more PC available for proper membrane function, improving liver lipid homeostasis, histology (H&E, Sudan red, Sirius red) and liver injury (ALT, AST).
Publication Title
Metabolomic Identification of Subtypes of Nonalcoholic Steatohepatitis.
Sample Metadata Fields
Age, Specimen part
View Samples- Zea mays
- 17 Downloadable Samples
- Illumina Genome Analyzer II
Description
We have generated over 80 million 32 nt reads generated from RNA samples isolated from the tip and base of a developing Mo17 leaf. A comparision of these data with the maize AGP resulted in the confirmation of approximately 88% of the maize filtered gene set Keywords: Transcriptome analysis Overall design: Examination of two different RNA samples from two different segments of a developing 3rd leaf
Publication Title
The B73 maize genome: complexity, diversity, and dynamics.
Sample Metadata Fields
Specimen part, Subject
View Samples- Zea mays
- 4 Downloadable Samples
- Illumina Genome Analyzer
Description
All above ground organs of higher plants are ultimately derived from shoot apical meristems (SAMs). The SAM exhibits distinctive structural organization, and monocot SAMs such as maize are comprised of two cell layers, a single cell layered tunica (L1) and a corpus (L2). Although recent research has revealed roles of these cell layers in the SAM, intra- and inter-cell-layer signaling networks involved in organ development remain largely unknown except for a few differentially expressed genes. Here, we used Illumnia technology to conduct RNA-seq of L1 and L2 cell layers in maize B73 maize shoot apical meristem. Overall design: Single sequencing library was constructed for L1 and L2 cell layer. Each library was sequenced using 2 lanes on a Solexa flow cell. Processed data file 'ZmB73_4a.53_filtered_genes.fasta' and its README file are linked below as supplementary files. The fasta file contains the gene model ID and corresponding sequence generated from maize genome project. This fasta file was used for the following samples: GSM418173, GSM418174, GSM420173, GSM420174, GSM422828, GSM422829.
Publication Title
The B73 maize genome: complexity, diversity, and dynamics.
Sample Metadata Fields
Age, Subject
View Samples