Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H3K9me3 and H3K27me3 ChIP-Seq in retinoblastoma 1 (RB1) knock out cells

ABSTRACT: Comparative analysis of H3K9me3 and H3K27me3 in RB1 KO and wild type IMR-90 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE173125 | GEO | 2021/12/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-Seq in retinoblastoma 1 (RB1) knock out IMR-90 cells

Project description:Total RNA-seq with rRNA depletion in retinoblastoma protein 1 knockout (RB1 KO) IMR-90

2021-12-29 | GSE173127 | GEO

RNA-Seq in retinoblastoma 1 (RB1) knock out IMR-90 cells

Project description:RNA-Seq in retinoblastoma 1 (RB1) knock out IMR-90 cells

| PRJNA723859 | ENA

H3K9me3 and H3K27me3 ChIP-Seq in retinoblastoma 1 (RB1) knock out cells

Project description:H3K9me3 and H3K27me3 ChIP-Seq in retinoblastoma 1 (RB1) knock out cells

| PRJNA723852 | ENA

UV-induced DNA lesion mapping in retinoblastoma 1 (RB1) knock out cells

Project description:In this study, we generated a human genome-wide map of DNA lesions induced by ultraviolet (UV) radiation in retinoblastoma knockout (RB1 KO) cells. Interestingly, we observed increased carcinogen susceptibility in closed HI-C domainS, pericentric and subtelomeric regions in RB1 KO. We also observed increased susceptibility at cancer driver loci such as TERT and TPTE. These loci are highly mutated in melanoma. Finally, we proposed that loss of tumor suppressor function can alter carcinogen susceptibility, and subsequently the mutation frequency of the genome.

2021-12-29 | GSE173126 | GEO

UV-induced DNA lesion mapping in retinoblastoma 1 (RB1) knock out cells

Project description:UV-induced DNA lesion mapping in retinoblastoma 1 (RB1) knock out cells

| PRJNA723855 | ENA

RB1 loss triggers dependence on ESRRG in retinoblastoma

Project description:Retinoblastoma (Rb) is a deadly childhood eye cancer that is classically initiated by inactivation of the RB1 tumor suppressor. Clinical management continues to rely on nonspecific chemotherapeutic agents that are associated with treatment resistance and toxicity. Here, we analyzed 103 whole exomes, 16 whole transcriptomes, 5 single-cell transcriptomes, and 4 whole genomes from primary Rb tumors to identify novel Rb dependencies. Several recurrent genomic aberrations implicate estrogen-related receptor gamma (ESRRG) in Rb pathogenesis. RB1 directly interacts with and inhibits ESRRG, and RB1 loss uncouples ESRRG from negative regulation. ESRRG regulates genes involved in retinogenesis and oxygen metabolism in Rb cells. ESRRG is preferentially expressed in hypoxic Rb cells in vivo. Depletion or inhibition of ESRRG causes marked Rb cell death which is exacerbated in hypoxia. These findings reveal a novel dependency of Rb cells on ESRRG, and they implicate ESRRG as a potential therapeutic vulnerability in Rb.

2022-08-24 | GSE196420 | GEO

ChIP-Seq, CPD-Seq and RNA-Seq in retinoblastoma 1 (RB1) knock out cells

Project description:ChIP-Seq, CPD-Seq and RNA-Seq in retinoblastoma 1 (RB1) knock out cells

| PRJNA723856 | ENA

Enhanced Innate Response In RB1 deficient Microglia Derived From Retinoblastoma Patient

Project description:Retinoblastoma (Rb), the most prevalent intraocular malignant tumor in children with global survival rate less than 30%, is mainly caused by the deficiency of the tumor suppressor RB1. A line of evidence have shown that local inflammation and immune escape play important roles in the occurrence of Rb, however the underlying mechanism remains unclear. We hypothesize that the unique neuroimmune cell type, retinal microglia, has a vital role in the Rb pathogenesis. In this study, we differentiated microglia cells (iMGs) from established induced pluripotent stem cells (iPSCs) derived from a retinoblastoma patient with the defined RB1 mutations. We investigated the function of RB1 in innate immune response of microglia and found that the expression of interleukins and chemokines, especially interleukin 6 and TNF-α, were highly upregulated in LPS-stimulated RB1 deficient iMGs, which enhanced innate immune responses and created a pro-inflammation environment. These findings demonstrated that RB1 is indispensable to maintain microglia function in innate immunity and its deficiency leads to enhanced inflammation responses, which may accelerate tumor growth and malignancy. This study provides new insights for pathological mechanism and immunotherapeutic target of retinoblastoma.

2022-12-31 | GSE212248 | GEO

Examining the effect of the linker DNA length on protein binding to di-nucleosomes decorated with H3K9me3 and H3K27me3

Project description:Characteristic features of chromatin states are not limited to particular epigenetic modifications but include other regulatory cues, such as linker DNA length, typically ranging from between 35-55 bp (Valouev et al, 2011; Voong et al., 2016, Cell) to over 200 bp in nucleosome-depleted regions (NDRs) found at active enhancers and promoters (Schones et al, 2008; Hansen He et al, 2010). To investigate whether and how the nucleosome linker DNA affects chromatin recognition by nuclear proteins we performed a set of affinity purifications using di-nucleosomes incorporating different DNA linkers. This dataset contains experiments aimed to probe how the linker DNA length affects protein binding to di-nucleosomes decorated with H3K9me3 or H3K27me3. The following di-nucleosomes were used in affinity pull-down purifications with HeLa nuclear extract followed by label-free MS: 1. unmod. H3, 35 bp linker 2. unmod. H3, 40 bp linker 3. unmod. H3, 45 bp linker 4. unmod. H3, 50 bp linker 5. unmod. H3, 55 bp linker 6. H3K9me3, 35 bp linker 7. H3K9me3, 40 bp linker 8. H3K9me3, 45 bp linker 9. H3K9me3 50 bp linker 10. H3K9me3, 55 bp linker 11. H3K27me3, 35 bp linker 12. H3K27me3, 40 bp linker 13. H3K27me3, 45 bp linker 14. H3K27me3, 50 bp linker 15. H3K27me3, 55 bp linker

2023-12-10 | PXD042368 | Pride

ChIP-Seq, CPD-Seq and RNA-Seq in retinoblastoma 1 (RB1) knock out cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-29 | GSE173128 | GEO