Ontology highlight
ABSTRACT:
PROVIDER: PRJNA993431 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Candidatus Electrothrix communis strain:RB | isolate:RB Genome sequencing
| PRJNA985436 | ENA
Project description:Comprehensive investigation of gene expression during fruit development and ripening in European pear (Pyrus communis).
2013-12-18 | GSE48393 | GEO
Project description:Candidatus Electrothrix sp. overview
| PRJNA1028703 | ENA
Project description:high throughput sequencing of the metagenome of mexican children
2020-03-16 | GSE143207 | GEO
Project description:Primary outcome(s): 68Ga-DOTA-GCC-RB PET/CT imaging
(Assessment of 68Ga-DOTA-GCC-RB PET/CT imaging to detect lesions in patients with colorectal carcinoma)Timepoint: 45 minutes to 1 hour from time of injection
| 29930 | ecrin-mdr-crc
Project description:The action of RB as a tumor suppressor has been difficult to define, in part, due to the redundancy of the related proteins p107 and p130. By coupling advanced RNAi technology with a genome wide analysis of gene expression and RB chromatin binding, we identified a unique and specific activity of RB in repressing DNA replication as cells exit the cell cycle into senescence, a tumor suppressive program. Binding of RB was examined in growing, quiescent, senescent or senescent cells lackign RB. Binding of p130 was examined in quiescent or senescent cells in the presence or absence of RB. Libraries were prapered from DNA co-precipiated with RB or p130 specific antibodies or from mock (beads-only) immunoprecipiates.
2010-01-15 | E-GEOD-19898 | biostudies-arrayexpress
Project description:Cell differentiation and proliferation are mutually exclusive. Although differentiating neurons are recognized as post-mitotic non-dividing cells, some Rb- and Rb family (Rb, p107, and p130)-deficient differentiating neurons proliferate and form tumor. Here, we found that the acute inactivation of all Rb family in differentiating cortical excitatory neurons caused radial migration defect and S-phase progression but not cell division, whereas that in cortical progenitors caused the cell division of the differentiating neurons generated from Rb –/–; p107 –/–; p130 –/– (Rb-TKO) progenitors. Genome-wide DNA methylation analysis revealed that proximal promoters tended to become methylated during differentiation in vivo. DNA demethylation by DNA methyltransferase inhibitor allowed the acutely inactivated Rb-TKO differentiating neurons to undergo G2/M-phase progression. Our finding illustrate that cortical excitatory neurons epigenetically lose their proliferative potency after neurogenesis. 1 sample of the V/SVZ tissue and the CP tissue
2014-01-01 | E-GEOD-37601 | biostudies-arrayexpress
Project description:RB’s interaction with chromatin is key to understanding its molecular functions. Using a novel ChIP-sequencing protocol, we identify the precise chromatin loci bound by various forms of human RB. RB targets three fundamentally different types of loci (promoters, enhancers, CTCF-sites), that are largely distinguishable by the mutually exclusive presence of E2F1, c-JUN and CTCF. E2F/DP facilitates RB association with promoters, whereas AP-1 recruits RB to enhancers. RB’s association with promoters and enhancers fluctuates: G1-arrest enriched RB at promoters, while S-phase progression redistributed RB towards enhancers. RB binding to RB/CTCF sites was unaltered by cell cycle progression. RB-bound promoters include the classic E2F targets and are similar between cell types. However, RB-bound enhancers are associated with different gene categories, including, notably, MAPK signaling, and they vary between cell types. We propose that RB has a well-preserved role controlling E2F in G1, and cell type-specific effects at enhancers when cells enter S-phase.
2022-08-01 | GSE176035 | GEO
Project description:We have done an expression experiment studying sexual dimorphism in gene expression in two species of songbirds, the zebra finch (Teaniopigia guttata) and the common whitethroat (Sylvia communis).
2010-11-30 | E-MEXP-2914 | biostudies-arrayexpress
Project description:The reprogramming of differentiated cells to an embryonic stem cell-like state provides a powerful system to explore fundamental mechanisms of development, including how mammalian cells establish and maintain pluripotency and long-term self-renewal capability. Based on the similarities between embryonic stem cells and cancer cells, we investigated the potential role of the retinoblastoma tumor suppressor and cell cycle regulator RB in the reprogramming of fibroblasts into induced pluripotent stem cells (iPS cells). Herein we demonstrate that loss of RB function leads to both an acceleration of the reprogramming process and the generation of more iPS clones from fibroblasts. This effect is largely due to a restrictive role for RB at the early stages of reprogramming. Surprisingly, however, RB inactivation does not enhance the formation of iPS clones by accelerating the proliferation of cells undergoing reprogramming. Rather, a genome-wide investigation of RB targets indicates that RB binds to regulatory regions of pluripotency genes such as Sox2 and Oct4 and contributes to their full repression in differentiated cells. This effect correlates with the maintenance of a repressive chromatin structure at these loci. Accordingly, Rb-deficient fibroblasts can be reprogrammed into iPS cells even in the absence of exogenous Sox2, which is normally required to initiate reprogramming from fibroblasts. These experiments identify a novel barrier in the reprogramming process, mainly the repression of certain pluripotency genes such as Sox2 by RB, which provides a new link between tumor suppressor mechanisms and cellular reprogramming. RNAseq from MEFs with 2 biological replicates (save CP), Rb ChIPseq from MEFs with 2 biological replicates, Histone H3 modification ChIPseq from MEFs with 1 biological replicate
2014-11-13 | E-GEOD-40594 | biostudies-arrayexpress