Transcriptome study of MX1 overexpression on down syndrome derived aminocytes(DSACs)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE237539 | GEO | 2024/01/02
REPOSITORIES: GEO
Similar Datasets
Project description:MX1 mediated AP-1 involved transcriptional regulation play an important role in the pathogenesis of DS through integration analysis of ATAC-seq and RNA-seq， therefore，AP-1 inhibition may be a potential therapeutic target for the treatment of DS-associated phenotye.
2024-01-02 | GSE237545 | GEO
Project description:Candidatus Methanomassiliicoccus intestinalis Issoire-Mx1 strain:Mx1-Issoire Genome sequencing
| PRJNA189659 | ENA
Project description:Transcriptome study of MX1 overexpression on down syndrome derived aminocytes(DSACs)
| PRJNA995604 | ENA
Project description:Endothelial progenitor cells were isolated from euploid and Down syndrome (DS) affected individuals. Gene expression was analyzed on total RNA extracted before or after infection with a human pathogen Bartonella hensaele. For euploid uninfected and infected cells, 2 biological replicates were performed. For DS isolated progenitors both infected and uninfected, a single microarray hybridization was performed. All hybridizations consists of three pooled samples each.
2010-01-12 | E-MTAB-312 | biostudies-arrayexpress
Project description:Acute megakaryoblastic leukemia (AMKL) is more frequently seen in Down syndrome patients, where it is often preceded by a transient myeloproliferative disorder (DS-TMD). The development of DS-TMD and DS-AMKL require not only the presence of the trisomy 21 but also that of GATA1 mutations. However, despite extensive studies into the genetics of DS-AMKL, not much is known about the epigenetic deregulation associated with this disease. In order to understand how epigenetic changes at the DNA methylation level contribute to DS leukemogenesis we performed DNA methylation profiling at different stages of development of this disease and analyzed the dynamics of epigenetic reprogramming. Early genome-wide epigenetic changes can be detected in trisomy 21 fetal liver mononuclear cells, even prior to the development of hematological abnormalities. These early changes are characterized by marked loss of DNA methylation at genes associated with regulation of key developmental processes. This first wave of aberrant DNA hypomethylation is followed by a second wave of epigenetic reprogramming detected in blast cells from DS-TMD and DS-AMKL, characterized by gains of methylation. This second wave of hypermethylation targets a distinct set of genes, preferentially affecting genes involved in hematopoiesis and regulation of cell growth and proliferation.
2013-08-19 | GSE46167 | GEO
Project description:Comprehensive gene expression assessment in prenatal DS lungs (n=19), and age-matched non-DS (n=19), was performed using high-throughput RNA sequencing (RNAseq)
2021-05-26 | GSE175539 | GEO
Project description:Results showed that Chd7 deficiency delay Cbfb-MYH11 induced leukemia, to explore the mechanism, We also performed microarray analysis on c-Kit+ leukemic cells to determine gene expression differences between Mx1-Cre, Cbfb+/56M and Chd7f/f, Mx1-Cre, Cbfb+/56M leukemic cells.
2018-02-14 | GSE103367 | GEO
Project description:Acute megakaryoblastic leukemia (AMKL) is more frequently seen in Down syndrome patients, where it is often preceded by a transient myeloproliferative disorder (DS-TMD). The development of DS-TMD and DS-AMKL require not only the presence of the trisomy 21 but also that of GATA1 mutations. However, despite extensive studies into the genetics of DS-AMKL, not much is known about the epigenetic deregulation associated with this disease. In order to understand how epigenetic changes at the DNA methylation level contribute to DS leukemogenesis we performed DNA methylation profiling at different stages of development of this disease and analyzed the dynamics of epigenetic reprogramming. Early genome-wide epigenetic changes can be detected in trisomy 21 fetal liver mononuclear cells, even prior to the development of hematological abnormalities. These early changes are characterized by marked loss of DNA methylation at genes associated with regulation of key developmental processes. This first wave of aberrant DNA hypomethylation is followed by a second wave of epigenetic reprogramming detected in blast cells from DS-TMD and DS-AMKL, characterized by gains of methylation. This second wave of hypermethylation targets a distinct set of genes, preferentially affecting genes involved in hematopoiesis and regulation of cell growth and proliferation. DNA methylation profiles obtained at different stages of the development of Down syndrome AMKL and from CD41+ cells from partial trisomic mice
2013-08-19 | E-GEOD-46167 | biostudies-arrayexpress
Project description:Patients with Down syndrome (DS) and acute lymphoblastic leukemia (ALL) have distinct clinical and biological features. Whereas most DS-ALL cases lack the sentinel cytogenetic lesions that guide risk assignment in childhood ALL, JAK2 mutations and CRLF2 overexpression are highly enriched. To further characterize the unique biology of DS-ALL, we performed genome-wide profiling of 58 DS-ALL and 35 non-Down syndrome (NDS) ALL cases by DNA copy number, loss of heterozygosity, gene expression, and methylation analyses. We report novel deletions within the 6p22 histone gene cluster as significantly more frequent in DS-ALL, occurring in 12 DS (24%) and only a single NDS case (3%) (Fisher’s exact p = 0.013). Homozygous deletions yielded significantly lower histone expression levels, and were associated with higher methylation levels, distinct spatial localization of methylated promoters, and enrichment of highly methylated genes for specific pathways and transcription factor binding motifs. Gene expression profiling identified CRLF2 overexpression in nearly half DS-ALL cases, and supervised analysis identified an associated 39-gene signature. However, no expression signature was identified for DS-ALL overall, nor for histone status, suggesting that DS-ALL constitutes several, heterogeneous molecular entities. Characterization of pathways associated with histone deletions and high CRLF2 expression may identify opportunities for novel targeted interventions. This SuperSeries is composed of the SubSeries listed below.
2011-07-12 | GSE21094 | GEO
Project description:Using Illumina 450K arrays, 1.85% of analyzed CpG sites were hypermethylated and 0.31% hypomethylated in fetal Down syndrome (DS) cortex throughout the genome. The vast majority of differentially methylated promoters and genes was hypermethylated in DS and located outside chromosome 21, including the γ-protocadherin (PCDHG) cluster on chromosome 5q31, which is crucial for neural circuit formation in the developing brain. Bisulfite pyrosequencing and targeted RNA sequencing showed that several genes of PCDHG subfamilies A and B are hypermethylated and transcriptionally downregulated in fetal DS cortex. Decreased PCDHG expression is expected to reduce dendrite arborization and growth in cortical neurons. Dysregulation of CPT1B and NOX5 may be associated with mitochondrial dysfunction and increased cell damage in the developing DS brain. Since constitutive hypermethylation of PCDHG and other genes affects multiple tissues, including blood, it may provide useful biomarkers for DS brain development and pharmacologic targets for therapeutic interventions.
2016-08-03 | GSE73747 | GEO