This SuperSeries is composed of the SubSeries listed below.
Hippo/Yap signaling controls epithelial progenitor cell proliferation and differentiation in the embryonic and adult lung.
Specimen part
View SamplesShhCre;Mst1/2flx/flx (Mst1/2 D/D) mice were generated to conditionally delete Mst1 and Mst2 from epithelial progenitors during lung morphogenesis. Lungs from E18.5 control and Mst1/2 D/D mice were mechanically and enzymatically dissociated to generate single cell suspension. Epcam(+) cells were isolated using magnetic microbeads.
Hippo/Yap signaling controls epithelial progenitor cell proliferation and differentiation in the embryonic and adult lung.
Specimen part
View SamplesComplete (whole) embryonic kidneys were dissected from wild type and Hoxa11, Hoxd11 compound null embryons throughout development. Targets from two biological replicates of each were generated and the expression profiles were determined using Affymetrix MOE430A and MOE430B arrays. Comparisons between normal and mutant and comparisons of development samples identified global patterns of gene regulation in kidney development
Comprehensive microarray analysis of Hoxa11/Hoxd11 mutant kidney development.
No sample metadata fields
View SamplesMLL-AF9 expression in normal human umbilical cord blood CD34+ cells leads to long-term proliferation of a myeloid progenitor cell with leukemogenic potential. Expression of a Core Binding Factor leukemia fusion (AML1-ETO or CBFbeta-SMMHC) in human CD34+ cells results in self-renewal of primitive progenitor cells with multilineage potential and stem cell ability, but these cells do not induce leukemia in immunodeficient mice. This comparative microarray study was initiated to determine how faithful these cell cultures are to the transcriptome of patient samples expressing each of these different fusion proteins, and to analyze the signaling pathways that are unique to CBF cultures and MLL-fusion cultures, with the hope of determining why the MLL-fusion cells are leukemogenic while the CBF cells are not.
Microenvironment determines lineage fate in a human model of MLL-AF9 leukemia.
No sample metadata fields
View SamplesE11.5 metanephric mesenchyme and ureteric bud were dissected from the E11.5 kidney rudiment using fine manual microdissection (ureteric bud only) or both fine manual microdissection and laser capture microdissection (metanephric mesenchyme) to define the gene expression profiles of these structures. Additionally, HoxA11, HoxD11 compound null E11.5 metanephric mesenchyme was obtained through laser capture microdissection allowing analysis of possible Hox targets in kidney development. Targets from multiple biological replicates of each were generated and the expression profiles were determined using Affymetrix MOE430_v2 arrays.
Comprehensive microarray analysis of Hoxa11/Hoxd11 mutant kidney development.
No sample metadata fields
View SamplesAML1-ETO expression in normal human umbilical cord blood CD34+ cells leads to long-term proliferation of an early self-renewing primitive progenitor cell with multilineage potential and stem cell ability, but these cells do not induce leukemia in immunodeficient mice. This comparative microarray study was initiated to determine the differences in the transcriptome of AML-ETO-expressing CD34+ cells after extended culture in vitro, using normal cord blood cells expanded for 6-8 weeks in vitro and subsequently purified for the CD34+ population as the control comparison.
p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death.
No sample metadata fields
View SamplesTotal pancreatic RNA was isolated from 3 week old NOD.scid, NOD, BDC2.5/NOD and BDC2.5/NOD.scid animals by GITC method. Targets were produced using standard Affymetrix procedures from about 10ug total RNA. The data from NOD.scid, NOD, BDC2.5/NOD and BDC2.5/NOD.scid Affymetrix MGU74Av2 cel files was converted into Robust Multi Array (RMA) text file for analysis using GeneSpring 6.1
No associated publication
No sample metadata fields
View SamplesAberrant co-expression of LMO2 and TAL1 is regularly found in T cell acute lymphoblastic leukemia (T-ALL). Here we describe a xenotransplant model for primary T-ALL cells derived from a patient who developed LMO2/TAL1 associated T-ALL after gene therapy for X-SCID (gamma c deficiency) due to insertional activation and a SIL-TAL1 fusion as an additional independent event. We identified a protein complex containing LMO2, TAL1 and E47 in the patients T-ALL cells. This complex functions as a transcription regulation complex in undifferentiated hematopoietic cells. However, its role in T-ALL is not fully understood. By comparative gene expression profiling we identified retinaldehyde dehydrogenase (RALDH2) as one of the genes which was highly up regulated in the primary T-ALL cells; the gene product was N-terminally truncated (RALDH2-T), but enzymatically active. To investigate the interference of LMO2 in RALDH2-T expression as well as the role of RALDH2-T in T-ALL development, LMO1 (analogue of LMO2) was down regulated by RNA interference in the T-ALL cell line Jurkat which led to a decrease of RALDH2-T expression and cell viability, indicating that positive regulation of RALDH2-T through an LMO1 or 2 containing transcription regulation complex might be essential for maintaining the T-ALL phenotype.
No associated publication
No sample metadata fields
View SamplesAnalysis of differential gene expression of total skin from different Notch signaling pathway mutants (specifically PSmut, RBPjmut, and PSRmut). Preselin1&2 are the core components of g-secretase enzyme which essential for the Notch receptor activation. RBPjk is the DNA-binding partner of the Notch Intracellular Domain. The hypothesis tested in the present study was RBPjmut skin would resemble the wild-type skin at the transcriptional level, since RBPjmut mice exhibit milder phenotype than PSmut or PSRmut mice.
No associated publication
Specimen part
View SamplesLeanness is associated with increased lifespan and is linked to favorable metabolic conditions promoting life extension.
Deficiency of the lipid synthesis enzyme, DGAT1, extends longevity in mice.
Sex, Specimen part
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