Exponentially growing cells and type II persister cells from the DS1-(hipQ)-strain
Novel protocol for persister cells isolation.
Specimen part, Disease, Cell line
View SamplesTHREE INDEPENDENT REPLICATES AND ARE THE CONTROL NON-INFECTED CELLS:
Modulation of NB4 promyelocytic leukemic cell machinery by Anaplasma phagocytophilum.
No sample metadata fields
View SamplesMembrane estrogen receptor (ER) alpha stimulates AMP kinase to suppress SREBP1 processing and lipids in liver
Estrogen reduces lipid content in the liver exclusively from membrane receptor signaling.
Specimen part
View SamplesPURPOSE
Gene expression profiling reveals novel biomarkers in nonsmall cell lung cancer.
Specimen part, Disease
View SamplesTo identify potential targets of miR-34a, we performed transcriptional profiling on proneural TS543 GBM cells, focusing on mRNAs whose levels decreased in response to miR-34a transfection as compared to control oligonucleotide.
miR-34a repression in proneural malignant gliomas upregulates expression of its target PDGFRA and promotes tumorigenesis.
Cell line, Treatment
View SamplesSystemic hypertension increases cardiac workload and subsequently induces signaling networks in heart that underlie myocyte growth (hypertrophic response) through expansion of sarcomeres with the aim to increase contractility. However, conditions of increased workload can induce both adaptive and maladaptive growth of heart muscle. Previous studies implicate two members of the AP-1 transcription factor family, junD and fra-1, in regulation of heart growth during hypertrophic response. In this study, we investigate the function of the AP-1 transcription factors, c-jun and c-fos, in heart growth. Using pressure overload-induced cardiac hypertrophy in mice and targeted deletion of Jun or Fos in cardiomyocytes, we show that c-jun is required for adaptive cardiac hyphertrophy, while c-fos is dispensable in this context. c-jun promotes expression of sarcomere proteins and suppresses expression of extracellular matrix proteins. Capacity of cardiac muscle to contract depends on organization of principal thick and thin filaments, myosin and actin, within the sarcomere. In line with decreased expression of sarcomere-associated proteins, Jun-deficient cardiomyocytes present disarrangement of filaments in sarcomeres and actin cytoskeleton disorganization. Moreover, Jun-deficient hearts subjected to pressure overload display pronounced fibrosis and increased myocyte apoptosis finally resulting in dilated cardiomyopathy. In conclusion, c-jun but not c-fos is required to induce a transcriptional program aimed at adapting heart growth upon increased workload.
The AP-1 transcription factor c-Jun prevents stress-imposed maladaptive remodeling of the heart.
No sample metadata fields
View SamplesPTPRD is a tumor suppressor of glioma that is frequently co-deleted with CDKN2A/p16. We show that Ptprd and p16 cooperate to promote gliomagenesis in the RCAS PDGFB / Nestin tv-A glioma mouse model.
Loss of the tyrosine phosphatase PTPRD leads to aberrant STAT3 activation and promotes gliomagenesis.
Specimen part
View SamplesBackground. The development of reliable gene expression profiling technology is having an increasing impact on our understanding of breast cancer biology.
Gene expression signatures in breast cancer distinguish phenotype characteristics, histologic subtypes, and tumor invasiveness.
Disease stage
View SamplesThe host immune response against an infection requires the coordinated action of many diverse cell subsets that dynamically adapt to the pathogen threat. Here we combined WGCNA and DCQ to analyse time-resolved mouse splenic transcriptomes in acute and chronic LCMV infections. This approach allowed to better characterize the dynamic cell events occurring in complex tissues such as the induction of the adaptive T cell response which requires the coordination of monocytes/macrophages and CD8+ T cells. Overall design: mRNA profiles of CD8 T cells and macrophages (in duplicate days 0 and 7 post-infection) from C57BL/6 mice infected with 2x10E2 pfu of LCMV strain Docile, generated by deep sequencing.
Linking Cell Dynamics With Gene Coexpression Networks to Characterize Key Events in Chronic Virus Infections.
No sample metadata fields
View SamplesBACKGROUND: miRNA have been shown to play an important role during immune-mediated diseases such as inflammatory bowel disease. The aim of this study was to assess differential expression of miRNA between uninfected and infected mice with Clostridium difficile strain VPI 10463 RESULTS: MicroRNA (miRNA)-sequencing analysis indicated that miR-146b, miR-1940, and miR-1298 were significantly overexpressed in colons of C. difficile-infected mice Overall design: Colon of uninfected and C.difficile-infected C57BL6/J WT mice were sampled at day 4 post-infection with Clostridium difficile VPI 10463. The infection dose was 107 cfu/mouse.
Modeling the role of peroxisome proliferator-activated receptor γ and microRNA-146 in mucosal immune responses to Clostridium difficile.
Specimen part, Cell line, Subject
View Samples