Ontology highlight
ABSTRACT:
PROVIDER: PRJNA343948 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression analysis of wid type and Lmnb1-/- epicardial cells
2017-01-01 | GSE87344 | GEO
Project description:Comparison of gene expression profiles in wild type cells vs Lmnb1 knockout cells.
2007-01-08 | E-MEXP-538 | biostudies-arrayexpress
Project description:The goal of this study was to compare the gene expression profile, using RNA-seq technology, of mouse epicardial-cells with Meis1-Meis2 double KO or wild-type genotypes.
2024-09-01 | GSE212504 | GEO
Project description:Senescence is a stress responsive form of stable cell cycle exit. Senescent cells have a distinct gene expression profile, which is often accompanied by the spatial redistribution of heterochromatin into senescence-associated heterochromatic foci (SAHFs). Studying a key component of the nuclear lamina, lamin B1 (LMNB1), we report dynamic alterations in its genomic profile and their implications for SAHF formation and gene regulation during senescence. Genome-wide mapping reveals that LMNB1 is depleted during senescence, preferentially from the central regions of lamina-associated domains (LADs), which are enriched for H3K9me3. LMNB1 knockdown facilitates the spatial relocalization of perinuclear H3K9me3, thus promoting SAHF formation, which is inhibited by ectopic LMNB1 expression. Furthermore, despite the global reduction in LMNB1 protein levels, LMNB1 binding increases during senescence in a small subset of gene-rich regions where H3K27me3 also increases and gene expression becomes repressed. These results suggest that LMNB1 may contribute to senescence in at least two ways due to its uneven genomewide redistribution: firstly through the spatial re-organization of chromatin and, secondly, through gene repression.
2013-08-22 | GSE49341 | GEO
Project description:Senescence is a stress responsive form of stable cell cycle exit. Senescent cells have a distinct gene expression profile, which is often accompanied by the spatial redistribution of heterochromatin into senescence-associated heterochromatic foci (SAHFs). Studying a key component of the nuclear lamina, lamin B1 (LMNB1), we report dynamic alterations in its genomic profile and their implications for SAHF formation and gene regulation during senescence. Genome-wide mapping reveals that LMNB1 is depleted during senescence, preferentially from the central regions of lamina-associated domains (LADs), which are enriched for H3K9me3. LMNB1 knockdown facilitates the spatial relocalization of perinuclear H3K9me3, thus promoting SAHF formation, which is inhibited by ectopic LMNB1 expression. Furthermore, despite the global reduction in LMNB1 protein levels, LMNB1 binding increases during senescence in a small subset of gene-rich regions where H3K27me3 also increases and gene expression becomes repressed. These results suggest that LMNB1 may contribute to senescence in at least two ways due to its uneven genomewide redistribution: firstly through the spatial re-organization of chromatin and, secondly, through gene repression. ChIP-seq for Lamin B1 in Growing and Ras Induced Senescence
2013-08-22 | E-GEOD-49341 | biostudies-arrayexpress
Project description:RNA-Seq based gene expression profiling of mouse epicardial-cells with Meis1-Meis2 double KO or wild-type genotypes.
| PRJNA875648 | ENA
Project description:This study addresses the mechanisms regulating the identity of oligodendrocyte progenitor cells (OPC) in physiological conditions and the pathological mechanisms leading to autosomal adrenoleukodystrophy (ADLD), a disease caused by persistence of lamin B1 (LMNB1) expression in oligodendrocytes (OL). Using mouse primary OPCs and a novel technique for the study of DNA-protein interaction, we identify the genomic regions showing dynamic interactions with LMNB1. The transition from ESC to OPC revealed increased association of gene involved in pluripotency and neuronal function and decreased association of gene categories associated with the differentiation of OPC into OL (including genes regulating epigenetic modifiers, RNA processing and protein phosphorylation). Since LMNB1 declines during the transition from OPC to OL, and its persistent expression has been linked to pathological conditions, such as ADLD, we further identified the molecular maps of genome-lamina reorganization in OPC differentiating into OL which continue to express LMNB1 (mOLLMNB1). The transition from OPC to mOLLMNB1 revealed increased association to LMNB1 of genomic regions encoding for lipid metabolism and protein phosphorylation, and decreased association of genes negatively regulating differentiation. These data highlight the importance of LMNB1 in physiological conditions and identify mechanisms responsible for late onset ADLD.
2020-03-16 | GSE135834 | GEO
Project description:This pilot study is being mounted to assess whether treatment assignment by ERCC-1 gene expression status suggests better clinical results from historical experience in metastatic colorectal cancer (mCRC). In wild type KRAS mCRC patients treated with either FOLFOX or FOLFIRI in combination with cetuximab the median response rate is approximately 60-65%. Biomarker directed treatment in this study may demonstrate that patients with low ERCC-1 treated with FOLFOX and cetuximab, and those with high ERCC-1 treated with FOLFIRI and cetuximab, will improve response rate to 70-75%. KRAS wild type patients will be treated with 6 cycles of one of the following regimens chosen for optimization based on patient characteristics (primary treatment phase). Patients with ERCC-1 < 1.7 relative gene expression of ERCC-1 over ß-actin (ERCC-1 low) will be assigned to treatment with mFOLFOX6 in combination with Cetuximab. Patients with ERCC-1 gene expression > 1.7 relative gene expression of ERCC-1 over over ß-actin (ERCC-1 high) will be assigned to treatment with FOLFIRI in combination with Cetuximab.
| 2133316 | ecrin-mdr-crc
Project description:Gene expression profiling of wild type and BMPR1a deficient aTreg cells
| PRJNA587140 | ENA
Project description:The most common cytogenetic abnormality found in complex karyotype high risk MDS/AML is del5q. Disease is often identified through visual inspection and recognition of abnormalities such as pseudo-Pelger-Huet anomaly (PPHA), which presents as deviations of normal neutrophil nuclear morphology. The link between PPHA and leukemia is unknown, but mutations in the lamin B1 receptor (LBR) have been identified as the cause of benign presence in otherwise normal individuals. Lamin B1 (LMNB1) is the ligand for LBR and is important for maintaining nuclear lamina integrity and influencing 3D gene structural changes that impact transcription; the LMNB1 gene locus is also contained with chromosome 5q, so we hypothesized that appearance of PPHA is potentially caused by del5q in MDS/AML containing the LMNB1. To help characterize the potential role of LMNB1 in normal hematopoietic stem and progenitor cells (HSPCs), we infected CD34+ cord blood HSPCs with lentiviruses expressing shRNAs targeting LMNB1 (LB1) and luciferase (C11) as a control and assessed changes in transcription due to LMNB1 disruption via RNSeq and 3D genome structural changes through HiC. Neutrophils were also differentiated from LMNB1 shRNA and control treated CD34+ cord blood HSPCs and transcriptional/structural changes identified via RNAseq and HiC. Additionally, to understand long-term in vivo effects of LMNB1 loss on self-renewal and lineage bias, we engrafted control and LMNB1 shRNA infected CD34+ HSPCs into NSG mice and harvest hCD34+ cells 12 weeks later for scRNAseq.
2022-03-11 | GSE174533 | GEO