Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA237651 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1165040.fastq.gz | Fastqsanger.gz | |||
| SRR1165050.fastq.gz | Fastqsanger.gz | |||
| SRR1165041.fastq.gz | Fastqsanger.gz | |||
| SRR1165051.fastq.gz | Fastqsanger.gz | |||
| SRR1165042.fastq.gz | Fastqsanger.gz |
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Project description:We analyzed the genome wide localization of H3K4me3, H3K27me3 and the NUP98-PHF23 (with V5 tag) fusion protein which binds H3K4me3 via its PHD finger, using ChIP-seq. Results correlated with gene expression profiles. NUP98-PHF23 bound only 1.6% of H3K4me3 marks including Hoxa/b + Meis1. Assess H3K4me3 and H3K27me3 histone marks, and correlate these marks with chromatin binding of the NP23 fusion protein using lymphoblast and myeloblast cell lines derived from NP23 leukemias.
2014-03-06 | E-GEOD-54786 | biostudies-arrayexpress
Project description:We analyzed the genome wide localization of H3K4me3, H3K27me3 and the NUP98-PHF23 (with V5 tag) fusion protein which binds H3K4me3 via its PHD finger, using ChIP-seq. Results correlated with gene expression profiles. NUP98-PHF23 bound only 1.6% of H3K4me3 marks including Hoxa/b + Meis1.
2014-03-06 | GSE54786 | GEO
Project description:NUP98-PHF23 is oncogenic and results in a Hoxa/b + Meis1 overexpression in NP23 leukemias and in premalignant (clinically healthy) hematopoietic tissues.
2014-03-06 | GSE54787 | GEO
Project description:NUP98-PHF23 is oncogenic and results in a Hoxa/b + Meis1 overexpression in NP23 leukemias and in premalignant (clinically healthy) hematopoietic tissues. Gene expression profiles from AML, pre-T LBL and B-ALL were compared to wild type bone marrow, thymus and spleen tissues respectively. Similarly, gene expression profiles from premalignant (clinically healthy) NP23 bone marrow, thymus and spleen were compared to wild type bone marrow, thymus and spleen tissues respectively. 106A and 748T lymphoblastic cell lines were compared to wild type thymic tissue.
2014-03-06 | E-GEOD-54787 | biostudies-arrayexpress
Project description:Gene expression study of leukemic and premalignant hematopoietic tissues from NUP98-PHF23 (NP23) mice.
| PRJNA237650 | ENA
Project description:Genome-wide maps of NUP98 fusion and MLL1 co-bound targets and their chromatin state in NUP98 fusion transformed cells.
| PRJNA305933 | ENA
Project description:Genome-wide maps of N_NUP98 and NUP98-TOP1 and MLL1 co-bound targets and their chromatin state in NUP98 fusion transformed cells.
| PRJNA325289 | ENA
Project description:The dysregulation of plant homeodomain (PHD) fingers has been implicated in several human diseases, including cancer. In a subset of aggressive acute myeloid leukemia (AML), chromosomal translocations that involve nucleoporin 98 (NUP98), a component of the nuclear pore complex, and a PHD finger-containing protein, such as KDM5A/JARID1A, PHF23 and BPTF, generate potent oncoproteins (namely NUP98-KDM5A, NUP98-PHF23 and NUP98-BPTF; or together termed as NUP98-PHD fusions) that are able to arrest hematopoietic differentiation and induce acute myeloid leukemia in murine models. In these processes, a PHD finger that specifically recognizes H3K4me3/2 marks was essential for leukemogenesis. Mutations in PHD fingers that abrogated H3K4me3 binding also abolished leukemic transformation. An overlap of NUP98-KDM5A oncoprotein binding sites and H3K4me3-positive loci at the Hoxa/b gene clusters and Meis1 in ChIP-seq together with NMR analysis of the H3K4me3-binding sites of the PHD fingers from PHF23, KDM5A and BPTF suggests a common PHD finger-dependent mechanism that promotes leukemogenesis by this type of NUP98-PHD finger fusions. Disulfiram (DS), a small molecule compound that directly targets the PHD finger, shows anti-proliferation effects in AML cells expressing NUP98-PHD through the conserved inhibitory mechanism. Our findings highlight the direct correlation between the abilities of NUP98-PHD finger fusion chimeras to associate with H3K4me3-enriched chromatin and leukemic transformation.
2020-07-13 | GSE146693 | GEO
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature