Z138-SNP_array_data
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE278105 | GEO | 2025/07/18
REPOSITORIES: GEO
Similar Datasets
Project description:Using chromatin conformation capture methods, we learned that the latent episome of the human Epstein-Barr virus (EBV) displays preferential chromosome association that correlates with gene density. The episome avoids gene-rich chromosomes and favors gene-poor chromosomes. Kaposi’s sarcoma-associated herpesvirus behaves similarly, but human papillomavirus does not, suggesting limited evolutionary conservation of this strategy. Moreover, the strongest contacts we detected between the human genome and EBV episome localized to OriP, the latent origin of replication. This genetic element, and the EBNA1 protein that binds there, are sufficient to reconstitute chromosome association preferences of the entire episome. Upon reactivation from latency, however, these preferences are lost. Detailed mapping of changes in interchromosomal contacts reveal that the episome moves away from repressive heterochromatin and toward activating euchromatin. Our work adds three-dimensional relocalization to the molecular events that occur during the genetic switch from EBV latency to reactivation. The involvement of only a myriad of interchromosomal contacts also argues for a possible role of this type of long-range association in gene regulation.
2017-11-13 | GSE98122 | GEO
Project description:Using chromatin conformation capture methods, we learned that the latent episome of the human Epstein-Barr virus (EBV) displays preferential chromosome association that correlates with gene density. The episome avoids gene-rich chromosomes and favors gene-poor chromosomes. Kaposi’s sarcoma-associated herpesvirus behaves similarly, but human papillomavirus does not, suggesting limited evolutionary conservation of this strategy. Moreover, the strongest contacts we detected between the human genome and EBV episome localized to OriP, the latent origin of replication. This genetic element, and the EBNA1 protein that binds there, are sufficient to reconstitute chromosome association preferences of the entire episome. Upon reactivation from latency, however, these preferences are lost. Detailed mapping of changes in interchromosomal contacts reveal that the episome moves away from repressive heterochromatin and toward activating euchromatin. Our work adds three-dimensional relocalization to the molecular events that occur during the genetic switch from EBV latency to reactivation. The involvement of only a myriad of interchromosomal contacts also argues for a possible role of this type of long-range association in gene regulation.
2017-11-13 | GSE98121 | GEO
Project description:Using chromatin conformation capture methods, we learned that the latent episome of the human Epstein-Barr virus (EBV) displays preferential chromosome association that correlates with gene density. The episome avoids gene-rich chromosomes and favors gene-poor chromosomes. Kaposi’s sarcoma-associated herpesvirus behaves similarly, but human papillomavirus does not, suggesting limited evolutionary conservation of this strategy. Moreover, the strongest contacts we detected between the human genome and EBV episome localized to OriP, the latent origin of replication. This genetic element, and the EBNA1 protein that binds there, are sufficient to reconstitute chromosome association preferences of the entire episome. Upon reactivation from latency, however, these preferences are lost. Detailed mapping of changes in interchromosomal contacts reveal that the episome moves away from repressive heterochromatin and toward activating euchromatin. Our work adds three-dimensional relocalization to the molecular events that occur during the genetic switch from EBV latency to reactivation. The involvement of only a myriad of interchromosomal contacts also argues for a possible role of this type of long-range association in gene regulation.
2017-11-13 | GSE98120 | GEO
Project description:Using chromatin conformation capture methods, we learned that the latent episome of the human Epstein-Barr virus (EBV) displays preferential chromosome association that correlates with gene density. The episome avoids gene-rich chromosomes and favors gene-poor chromosomes. Kaposi’s sarcoma-associated herpesvirus behaves similarly, but human papillomavirus does not, suggesting limited evolutionary conservation of this strategy. Moreover, the strongest contacts we detected between the human genome and EBV episome localized to OriP, the latent origin of replication. This genetic element, and the EBNA1 protein that binds there, are sufficient to reconstitute chromosome association preferences of the entire episome. Upon reactivation from latency, however, these preferences are lost. Detailed mapping of changes in interchromosomal contacts reveal that the episome moves away from repressive heterochromatin and toward activating euchromatin. Our work adds three-dimensional relocalization to the molecular events that occur during the genetic switch from EBV latency to reactivation. The involvement of only a myriad of interchromosomal contacts also argues for a possible role of this type of long-range association in gene regulation.
2017-11-13 | GSE98498 | GEO
Project description:Immunocytochemical studies revealed that dG9a moves into nucleus after cycle 8 and appears to regulate gene expression by di-methylating H3K9 from cycle 8 to cycle 11. To determine which genes are regulated by dG9a during cycles 8-11, we examined mRNA levels by performing RNA-sequence analysis using early embryos (0-2 h after egg laying) of dG9a null mutant and wild type as a control
2015-08-01 | GSE56665 | GEO
Project description:Recent studies in our lab have identified a mutant mouse model of obstructive nephropathy designated mgb for megabladder. Homozygotic mgb mice (mgb-/-) develop lower urinary tract obstruction in utero due to a lack of bladder smooth muscle differentiation. This defect is the result of a random transgene insertion into chromosome 16 followed by a translocation of this fragment into chromosome 11. In an effort to identify potential gene targets affected in mgb mice, we performed transcriptional profiling on embryonic day 15 (E15) mgb-/- bladders using both a Chromosome 11/16 Custom GeneChip Array and the Affymetrix Mouse Genome 430 2.0 GeneChip. This analysis identified no definitive mis-expressed gene targets on chromosome 11. In contrast, mgb-/- mice significantly over-expressed a cluster of gene products located on the translocated fragment of chromosome 16 including urotensin II-related peptide (Urp), which was shown to be preferentially over-expressed in developing mgb-/- bladders. Immunohistochemical studies indicated that the spatial distribution of Urp was altered in mgb-/- bladders, while biochemical studies suggested a potential role for Urp in modifying smooth muscle cell phenotype in vitro. Pathway analysis of mgb microarray data showed dysregulation of at least 60 gene products associated with the differentiation of smooth muscle. In conclusion, the results of this study indicate that the molecular pathways controlling normal smooth muscle development are severely altered in mgb-/- bladders, and provide the first evidence that Urp may play a critical role in bladder smooth muscle development. Keywords: mgb mutant bladders
2007-08-09 | GSE8715 | GEO
Project description:We identified a congenic mouse with an introgressed region from the A/J donor inbred strain on an inbred C57BL/6J background that showed a reduced locomotor stimulant response to methamphetamine. We conducted microarray analysis of the striatum from drug-naive female and male mice that were 6-9 weeks old. The congenic region is on chromosome 11 and spans approximately 84-96 Mb. There were two groups of mice used in the analysis: B6 control mice versus congenic mice. Congenic mice were collapsed across heterozygous and homozygous genotypes. All mice are on a C57BL/6J background. Congenic mice differ only on chromosome 11 where they contain the introgressed A/J alleles from 84-96 Mb.
2012-01-18 | GSE35139 | GEO
Project description:Immunocytochemical studies revealed that dG9a moves into nucleus after cycle 8 and appears to regulate gene expression by di-methylating H3K9 from cycle 8 to cycle 11. To determine which genes are regulated by dG9a during cycles 8-11, we examined mRNA levels by performing RNA-sequence analysis using early embryos (0-2 h after egg laying) of dG9a null mutant and wild type as a control mRNA profiles of about 0-2h-old embryos of wild type (CantonS) and dG9a-depleted (dG9aRG5) strain
2015-08-01 | E-GEOD-56665 | biostudies-arrayexpress
Project description:The translocation t(11;14) occurs in 20% of multiple myeloma (MM) patients and results in the upregulation of CCND1. Nearly two-thirds of t(11;14) MM cells are BCL2 primed and highly responsive to the oral BCL2 inhibitor venetoclax. While it is evident that this unique sensitivity to venetoclax depends on the BH3-proapoptotic protein priming of BCL2, the biology underlying t(11;14) MM dependency on BCL2 is poorly defined. Importantly, the epigenetic regulation of t(11;14) transcriptomes and its impact on gene regulation and clinical response to venetoclax remains elusive. In this study, by integrating ATACseq and RNAseq at the single-cell level in primary MM samples, we have defined the epigenetic regulome and transcriptome associated with t(11;14) MM. A "B cell-like" epigenetic signature was enriched in t(11;14) MM, confirming its phylogeny link to B cell rather than plasma cell biology. Of note, a loss of a "B cell-like" epigenetic signature with a gain of canonical plasma cell transcription factors was observed at the time of resistance to venetoclax. In addition, MCL1 and BCL2L1 copy number gains and structural rearrangements were linked to venetoclax resistance in t(11;14) MM patients. To date, this is the first study in which both scATAC-seq and scRNA-seq analysis are integrated into primary MM cells to obtain a deeper resolution of the epigenetic regulome and transcriptome associated with t(11;14) MM biology and venetoclax resistance.
2023-09-21 | GSE199372 | GEO