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GSE7656
Escherichia coli
18 Downloadable Samples
Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
We probed the mechanism of cross-regulation of osmotic and heat stress responses by characterizing the effects of high osmolarity (0.3M vs. 0.0M NaCl) and temperature (43oC vs. 30oC) on the transcriptome of Escherichia coli K12 using E. coli Genome 2 Array (Affymetrix, Inc.). Independent array hybridizations were carried out for 3 biological replicates (independent cultures). Total RNA was extracted using a hot phenol-chloroform method. cDNA synthesis, fragmentation and labeling, and washing and scanning of E. coli GeneChip Arrays were performed according to the instructions of the manufacturer (Affymetrix Technical Manual, Affymetrix, Inc., USA). Labeled cDNA was hybridized to E. coli Genome 2 Array (Affymetrix, Inc.). Independent array hybridizations were carried out for 3 biological replicates (independent cultures) of each condition. A number of genes in the SoxRS and OxyR oxidative stress regulons were up-regulated by high osmolarity, high temperature, and/or by the combination of both stresses. This result could account for cross-protection of osmotic stress against oxidative stress. The trehalose biosynthetic genes were induced by both stresses, in accord with the proposed protective role of this disaccharide against thermal and oxidative damage.
Publication Title
Genome-wide transcriptional responses of Escherichia coli K-12 to continuous osmotic and heat stresses.
Sample Metadata Fields
No sample metadata fields
View Samples- Escherichia coli
- 6 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
DNA microarrays were conducted on E. coli K12 cells stressed with 10 M in N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN). Overall, 260 genes varied in expression, 114 up-regulated and 146 down-regulated by Zn deprivation
Publication Title
Characterization of Zn(II)-responsive ribosomal proteins YkgM and L31 in E. coli.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina HiSeq 2000
Description
We used RNA-Seq to detail the global expression changes induced when SWELL1 is genetically deleted from adipocytes. Overall design: We generated isogenic SWELL1 KO adipocyte cell lines from 3T3-F442A cells. CRISR/Cas9 was used to knockout the SWELL1 gene in the parental 3T3-F442A line. These cell lines were grown in culture and RNA was extracted for sequencing. RNA was sequenced on an Illumina Hi-Seq at the University of Iowa Core Facility.
Publication Title
SWELL1 is a regulator of adipocyte size, insulin signalling and glucose homeostasis.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 2500
Description
In acute myeloid leukemia, chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that transgenic Mef2cS222A/S222A mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9. MEF2C phosphorylation was required for leukemia stem cell maintenance, induced by MARK kinases in cells, and blocked by selective MARK inhibitor MRT199665, which caused apoptosis of MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C. These findings identify signaling-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease. Overall design: RNA-sequencing of human leukemia cell line with induction of wildtype or mutant MEF2C.
Publication Title
MEF2C Phosphorylation Is Required for Chemotherapy Resistance in Acute Myeloid Leukemia.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
In acute myeloid leukemia, chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that transgenic Mef2cS222A/S222A mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9. MEF2C phosphorylation was required for leukemia stem cell maintenance, induced by MARK kinases in cells, and blocked by selective MARK inhibitor MRT199665, which caused apoptosis of MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C. These findings identify signaling-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease. Overall design: RNA-sequencing of human leukemia cell line with treatment of MARK inhibitor MRT199665.
Publication Title
MEF2C Phosphorylation Is Required for Chemotherapy Resistance in Acute Myeloid Leukemia.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus, Homo sapiens, Rattus norvegicus
- 15 Downloadable Samples
Illumina ratRef-12 v1.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Molecular Liver Cancer Prevention in Cirrhosis by Organ Transcriptome Analysis and Lysophosphatidic Acid Pathway Inhibition.
Sample Metadata Fields
Sex, Specimen part, Disease, Treatment
View Samples- Mus musculus
- 15 Downloadable Samples
- Illumina ratRef-12 v1.0 expression beadchip
Description
Gene-expression profiles of liver tissue of cabon tetrachloride (CCl4)-treated and control mice were obtained before and after organotypic ex vivo tissue culture.
Publication Title
Molecular Liver Cancer Prevention in Cirrhosis by Organ Transcriptome Analysis and Lysophosphatidic Acid Pathway Inhibition.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Aberrant TGFbeta signalling is a hallmark of epithelial derived tumours. Signalling patterns can depend on the membrane trafficking and internalization of the TGFbeta receptors. Protein kinase C (PKC), particularly the atypical PKC isoforms, alter the trafficking of TGFbeta receptors and can alter TGFbeta induced gene expression.
Publication Title
aPKC alters the TGFβ response in NSCLC cells through both Smad-dependent and Smad-independent pathways.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
miR-34c inhibits Dicer/Pten double knockout mouse serous epithelial cancer cell proliferation by inducing cell cycle arrest and apoptosis. We found that miR-34c had a more dramatic effect on inhibiting tumor cell viability than let-7b. The action of miR-34c induced tumor cell cycle arrest in G1 phase and apoptosis and was accompanied with the regulation of key genes involved in cell proliferation and cell cycle G1/S transition. miR-34c suppressed the expression of EZH2 and MYBL2, which may transcriptionally and functionally activate CDKN1C.
Publication Title
Functional analysis of miR-34c as a putative tumor suppressor in high-grade serous ovarian cancer.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 141 Downloadable Samples
- Illumina HiSeq 2500
Description
Tuberculosis (TB) is responsible for the majority of mortality and morbidity associated with infectious diseases worldwide. The characterization of exact molecular components of immune response associated with protection against TB may help design more effective therapeutic interventions. In this study, we aimed to characterize the immune signature of memory T cells associated with latent infection with Mycobacterium tuberculosis. Transcriptomic profiling using RNA sequencing was performed on memory CD4 and CD8 T cells isolated from individuals with latent tuberculosis, as well as from tuberculosis negative healthy controls. Overall, we found specific gene signatures in each cell subset that could successfully discriminate between individuals with latent tuberculosis and healthy controls. Overall design: RNA-sequencing of sorted memory CD4 and CD8 T cells from cryopreserved PBMC of 10 subjects with latent tuberculosis infection and 10 tuberculosis negative healthy controls
Publication Title
Circulating T cell-monocyte complexes are markers of immune perturbations.
Sample Metadata Fields
Disease, Disease stage, Subject
View Samples