This SuperSeries is composed of the SubSeries listed below.
AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes.
Specimen part, Disease
View SamplesGlucocorticoids (GCs) and protein kinase A (PKA)-activating agents (beta-adrenergic receptor agonists) are mainstream asthma therapies based on their ability to prevent or reverse excessive airway smooth muscle (ASM) constriction. Their abilities to regulate another important feature of asthma - excessive ASM growth are poorly understood. Recent studies have suggested that GCs render agents of inflammation such as interleukin 1beta and tumor necrosis factor alpha mitogenic to ASM, via suppression of (antimitogenic) induced cyclooxygenase-2-dependent PKA activity. To further explore the mechanistic basis of these observations, we assessed the effects of epidermal growth factor and interleukin 1beta stimulation, and the modulatory effects of GC treatment and PKA inhibition, on the ASM transcriptome by microarray analysis.
Glucocorticoid- and protein kinase A-dependent transcriptome regulation in airway smooth muscle.
No sample metadata fields
View SamplesSingle-cell analysis of KPC pancreatic tumor cells Overall design: Evaluate the single-cell transcriptomic landscape in 3 KPf/fC tumors
A Multiscale Map of the Stem Cell State in Pancreatic Adenocarcinoma.
Specimen part, Cell line, Subject
View SamplesmPDAC tumors of KPC mice Overall design: medium and large size tumors
A Multiscale Map of the Stem Cell State in Pancreatic Adenocarcinoma.
Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.
Specimen part, Disease, Disease stage, Cell line
View SamplesThe MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system.
Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.
Specimen part, Disease, Disease stage
View SamplesThe MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system.
Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.
Disease, Disease stage, Cell line
View SamplesWe report Illumina next generation RNA sequencing (RNAseq) of MLL-AF9 in vitro transformed murine LSKs upon genetic deletion of Mof. These gene expression data illustrate that Mof regulates the expression of genes involved in DNA damage response and chromatin stability in MLL-AF9 transformed cells. Overall design: RNAseq comparing Mof homozygous knockout cells to Mof wild type control
Histone Acetyltransferase Activity of MOF Is Required for <i>MLL-AF9</i> Leukemogenesis.
Cell line, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.
Specimen part, Cell line, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia.
Specimen part, Cell line, Treatment, Time
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