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SRP150759
Homo sapiens
6 Downloadable Samples
NextSeq 500
Description
Undifferentiated and differentiated Keratinocytes (AG1478 treated) were stained with antibody-RNA conjugates to measure protein-based diffrentiation changes in conjunction with single-cell transcriptomics. The cells were crosslinked and stained according to the RAID procedure to allow intracellular immunostaining. Antibodies used in this experiment are (TGM1, NOTCH1, KLK6, JAG1, phospho-RPS6, phospho-FAK). Overall design: Three 384 wells plates for untreated and Three 384 wells plates for AG1478 treated cells were processed for single cell transcriptomics
Publication Title
Combined quantification of intracellular (phospho-)proteins and transcriptomics from fixed single cells.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- NextSeq 500
Description
Cell fixation, permeabilization and antibody staining of could have adverse effects on the quality of single cell transcriptomics data. To assess the effects of the RAID procedure, which includes such steps, we performed a direct comparison of single cell transcriptomics by CELseq2 using unfixed and RAID-processed cells. Quality measures (gene complexity, gene detection rate, average gene expression) were performed using 40000 samples UMI counts per cell. Overall design: Single cells were sorted in 96, wells plates. Per condition (unfixed or RAID) three sets (A,B,C) of 48 cells were processed with the CELseq2 protocol.
Publication Title
Combined quantification of intracellular (phospho-)proteins and transcriptomics from fixed single cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- NextSeq 500
Description
Undifferentiated and differentiated Keratinocytes (AG1478 treated) were stained with antibody-RNA conjugates (targeting EGFR and ITGA6) to measure protein-based differentiation changes in conjunction with single-cell transcriptomics. Overall design: Two 384 wells plates for untreated and two 384 wells plates for AG1478 treated cells were processed for single cell transcriptomics.
Publication Title
Combined quantification of intracellular (phospho-)proteins and transcriptomics from fixed single cells.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. apolipoprotein E (apoE)-deficient mice, which develop heart failure at an age of 18 months, and non-transgenic C57BL/6J (B6) mice with heart failure triggered by 6 months of pressure overload induced by abdominal aortic constriction (AAC). The development of heart failure was monitored by echocardiography, invasive hemodynamics and histology. The microarray gene expression study of cardiac genes was performed with heart tissue from failing hearts relative to hypertrophic and healthy heart tissue, respectively. The microarray study revealed that the onset of heart failure was accompanied by a strong up-regulation of cardiac lipid metabolism genes involved in fat synthesis, storage and oxidation.
Publication Title
Up-regulation of the cardiac lipid metabolism at the onset of heart failure.
Sample Metadata Fields
Age, Specimen part, Disease
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E (apoE)- deficient mice as a model of atherosclerosis-induced heart failure to analyze whether the anti-ischemic drug ranolazine could retard the progression of heart failure. The study showed that 2 months of ranolazine treatment improved cardiac function of 18 month-old apoE-deficient mice with symptoms of heart failure as assessed by echocardiography. To identify changes in cardiac gene expression induced by treatment with ranolazine a microarray study was performed with heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts. The microarray approach identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine.
Publication Title
Up-regulation of the cardiac lipid metabolism at the onset of heart failure.
Sample Metadata Fields
Age, Specimen part, Disease, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril.
Publication Title
Angiotensin-converting enzyme inhibition down-regulates the pro-atherogenic chemokine receptor 9 (CCR9)-chemokine ligand 25 (CCL25) axis.
Sample Metadata Fields
Specimen part, Disease, Treatment
View Samples- Homo sapiens
- 5 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
miR-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem Cells.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 5 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
In acute myeloid leukemia (AML), leukemia stem cells (LSCs) play a central role in disease progression and recurrence due to their intrinsic capacity for self-renewal and chemotherapy resistance. Whereas epigenetic regulation balances normal blood stem cell self-renewal and fate decisions, mutation and dysregulation of epigenetic modifiers are now considered fundamental to leukemia initiation and progression. Alterations in miRNA function represent a non-canonical epigenetic mechanism influencing malignant hematopoiesis; however, the function of miRNA in LSC remains undetermined. Here we show that miRNA profiling of fractionated AML populations defines an LSC-specific signature that is highly predictive of patient survival. Gain-of-function genetic analysis demonstrated that miR-126 restrained cell cycle progression, prevented LSC differentiation, and increased LSC self-renewal. miR-126 promoted chemo-resistance, preserving LSC quiescence in part through suppression of the G0-to-G1 gatekeeper, CDK3. Thus, in AML, miRNAs influence patient outcome through post-transcriptional regulation of stemness programs in LSC.
Publication Title
miR-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem Cells.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 8 Downloadable Samples
- NextSeq 500
Description
We report transcriptomes of myofibroblasts from mouse skin wounds. Myofibroblasts were FACS sorted as Zombie-neg;tdTomato-hi cells from Sm22-Cre;TdTomato mice. We identified and analyzed 4,120 differentially expressed transcripts across four post-wounding time points, day 12, day 15, day 21 and day 26. Overall design: Examination of FACS sorted wound myofibroblasts from four consecutive post-wounding time points
Publication Title
Regeneration of fat cells from myofibroblasts during wound healing.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Testicular and ovarian gene expression changes with loss of DMXL2
Publication Title
Dual role of DMXL2 in olfactory information transmission and the first wave of spermatogenesis.
Sample Metadata Fields
Specimen part
View Samples