Dicer1 loss in the aP2-lineage leads to the development of aggressive and highly penetrant angiosarcomas independent of other oncogenes or tumor suppressor loss
Biallelic <i>Dicer1</i> Loss Mediated by <i>aP2-Cre</i> Drives Angiosarcoma.
Specimen part
View SamplesGenetic fate mapping was preformed on aP2-Cre;tdTomato and aP2-Cre;tdTomato;SmoM2/+ animals and endothelial progenitor cells identified as the cell of origin of FN-RMS in aP2-Cre;SmoM2/+ animals
Hedgehog Pathway Drives Fusion-Negative Rhabdomyosarcoma Initiated From Non-myogenic Endothelial Progenitors.
Specimen part
View SamplesGenes regulated by miR-206 were identified by microarray analysis in RD cells transfected with a Negative Control (NC) or miR-206 Mimic
PAX7 is a required target for microRNA-206-induced differentiation of fusion-negative rhabdomyosarcoma.
Specimen part, Cell line, Time
View SamplesActivation of Sonic Hedgehog signaling through expression of a constitutively active Smoothened allele under control of an aP2 adipocyte-restricted transgene in mice gives rise to aggressive skeletal muscle tumors that display the histologic and molecular characteristics of human embryonal rhabdomyosarcoma with high penetrance.
A mouse model of rhabdomyosarcoma originating from the adipocyte lineage.
Specimen part
View SamplesAE9aId1fl/flCreER cells treated with the control vehicle, CBD or 4-OHT Overall design: We treated AE9aId1fl/flCreER leukemia with 0.1 µM 4-hydroxytamoxifen (4-OHT) for 48 hours or the Id1 inhibitor CBD (at 15 µM) for 16 hours, and isolated RNA for RNA-seq analysis.
Regulation of AKT signaling by Id1 controls t(8;21) leukemia initiation and progression.
No sample metadata fields
View Samplescompare the gene expression profile between cep701 treated HEL cells with shPRMT5 knockingdown HEL cells. HEL cells contain homologous alells with mutation Jak2V617F. We found JAK2V617F can inactivate PRMT5 activity by directly phosphorylating PRMT5 through histone methylation.
JAK2V617F-mediated phosphorylation of PRMT5 downregulates its methyltransferase activity and promotes myeloproliferation.
Cell line, Treatment
View SamplesCompare the gene expression profile among human CD34+ cord blood cells infected with MIGR1, MIGR1-AML1-ETO or MIGR1-AML1-ETONHR1
The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation.
Specimen part
View SamplesWe observed that mutations in CBP60a, CML46, CML47 and WRKY70 enhanced plant resistance to Pma likely through different mechanisms. To investigate their contributions to enhanced resistance at the transcriptome level, we designed this experiment to measure their response to Pma using the SMART-3Seq method. Overall design: Mature leaves of Arabidopsis plants of seven different genotypes were infiltrated with mock or Pma. Samples were collected 24 hours after treatment. Each experiment contains one sample consisted of two leaves for each genotype-treatment combination. In total three independent experiments were conducted.
WRKY70 prevents axenic activation of plant immunity by direct repression of SARD1.
Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.
Age, Specimen part, Treatment
View SamplesAnalysis of brown adipose tissue from Yin Yang 1 (YY1) brown fat specific knockout mice fed a high fat diet for 3 months. YY1 deficiency in brown adipose tissue leads to strong thermogenic deficiency. The goal was to identify the genes controlled by YY1 responsible of brown fat defective function.
Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.
Age, Specimen part, Treatment
View Samples