Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA175421 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE40734: The effect on gene expression of Smchd1 deletion in primary MEFs, transformed MEFs and MEF tumours GSE40879: The effect on gene expression of Smchd1 deletion in pre-B cells from E17.5 Eµ-Myc embryos GSE40880: The effect on gene expression of Smchd1 deletion in end stage lymphomas GSE40881: The effect on gene expression of Smchd1 deletion in premalignant pre-B cells Refer to the individual subSeries. NOTE: all the cell types need to be analyzed separately.
2012-09-30 | E-GEOD-40992 | biostudies-arrayexpress
Project description:Smchd1 appears to act as a tumour suppressor in the Eµ-Myc mouse B cell lymphoma model. We find a small number of gene expression differences at E17.5 in the pre-B cells, before phenotypic differences are observed. The microarrays compared Smchd1 null and Smchd1 wildtype E17.5 preB cell samples. All samples are on the C57BL/6 background and carry the Eµ-Myc transgene, and the Smchd1 null samples are additionally homozygous for a Smchd1 genetrap allele.
2012-09-30 | E-GEOD-40879 | biostudies-arrayexpress
Project description:Smchd1 appears to act as a tumour suppressor in the Eµ-Myc mouse B cell lymphoma model. We find a small number of gene expression differences at E17.5 in the pre-B cells, before phenotypic differences are observed.
2012-09-30 | GSE40879 | GEO
Project description:Smchd1 appears to act as a tumour suppressor in the Eµ-Myc B cell lymphoma model. We find gene expression differences are most pronounced in premalignant cells. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis. The microarrays compared Smchd1 null and Smchd1 wildtype samples from premalignant pre-B cells. All samples are on the C57BL/6 background, and carry the Eµ-Myc transgene. Smchd1 null samples are additionally homozygous for a Smchd1 genetrap allele.
2012-09-30 | E-GEOD-40881 | biostudies-arrayexpress
Project description:Smchd1 appears to act as a tumour suppressor in the Eµ-Myc B cell lymphoma model. We find gene expression differences are most pronounced in the premalignant cells, and observe more variability in end stage lymphomas. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis. The microarrays compared Smchd1 null and Smchd1 wildtype samples from end stage lymphomas. All lymphomas are on the C57BL/6 background and carry the Eµ-Myc transgene, and Smchd1 null samples are additionally homozygous for a Smchd1 genetrap allele.
2012-09-30 | E-GEOD-40880 | biostudies-arrayexpress
Project description:The effect on gene expression of Smchd1 deletion in premalignant pre-B cells
| PRJNA175422 | ENA
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
2007-06-30 | GSE7162 | GEO
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Hearts were taken from wide type and Myc-null Mouse embryos at E13.5 under the dissecting scope. Cardiac myocyte RNA was isolated using TRIZOL®Reagent Total RNA (100 ng) was hybridized to the Sentrix® MouseRef-8 Expression BeadChip that contains probes for ~24,000 transcripts. GeneChips were scanned using the Hewlett-Packard GeneArray Scanner G2500A. The data were analyzed with Illumina Inc. BeadStudio version 1.5.0.34 and normalized by rank invariant method.
2010-06-10 | E-GEOD-7162 | biostudies-arrayexpress
Project description:Genome-wide analysis of gene expression in Eµ-Myc and Eµ-Myc Wrn Δhel/Δhel murine lymphomas
| PRJNA134213 | ENA
Project description:Many lymphoid malignancies arise from deregulated c-MYC expression in cooperation with additional genetic lesions. While many of these cooperative genetic lesions have been discovered and their functions characterised, DNA sequence data of primary patient samples suggest that many more do exist. However, the nature of their contributions to c-MYC driven lymphomagenesis have not yet been investigated. We identified TFAP4 as a potent suppressor of c-MYC driven lymphoma development in a previous genome-wide CRISPR knockout screen in primary cells in vivo. CRISPR deletion of TFAP4 in Eµ-MYC transgenic haematopoietic stem and progenitor cells (HSPCs) and transplantation of these manipulated HSPCs into lethally irradiated animals significantly accelerated c-MYC-driven lymphoma development. Interestingly, TFAP4 deficient Eµ-MYC lymphomas all arose at the pre-B cell stage of B cell development. This observation prompted us to characterise the transcriptional profile of pre-B cells from pre-leukaemic mice transplanted with Eµ-MYC/Cas9 HSPCs that had been transduced with sgRNAs targeting TFAP4. This analysis revealed that TFAP4 deletion reduced expression of several master regulators of B cell differentiation, such as Spi1, SpiB and Pax5, which are direct target genes of both TFAP4 and MYC. We therefore conclude that loss of TFAP4 leads to a block in differentiation during early B cell development, thereby accelerating c-MYC-driven lymphoma development.
2023-03-12 | GSE225684 | GEO