P53 and rH2AX enrichment in overexpressed SNCA on SHSY5Y
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA629122 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This study was designed to determine P53 and rH2AX regulated genes after a-synuclein expression. Our results showed that many genes involved in apoptosis and cellular senescence are directly regulatd by P53. rH2AX binding was more complex in that a-synuclein expression showed a change from random binding to specific bindings in certain promoters.
2022-03-09 | GSE149558 | GEO
Project description:Overexpressed SNCA in differentiated SH-SY5Y neuroblastoma cells
| PRJNA629117 | ENA
Project description:Transcriptome analysis of overexpressed SNCA in differentiated SH-SY5Y neuroblastoma cells
| PRJNA629121 | ENA
Project description:single cell polyA+ and total RNA-seq data was generated for NGP, SK-N-BE-2C and SHSY5Y-MYCN-TR cells
2019-01-01 | GSE119982 | GEO
Project description:SHSY5Y cells grown in MEM:F12 media (1:1) were treated with Endosulfan and total RNA was isolated from cells after 24 hour exposure Three replicate were used for the experiment
2016-01-01 | GSE65140 | GEO
Project description:TDP-43 is an important RNA binding protein. To better understand its binding targets in human neurons, we performed TDP-43 iCLIP on SHSY5Y cells.
2022-02-02 | E-MTAB-11243 | biostudies-arrayexpress
Project description:To determine sensitivity of a custom 8x60k aCGH design for mosaicism of SNCA gains, a peripheral blood lymphocyte (PBL) DNA sample with a known heterozygous duplication (CN 3, or 50% increase in SNCA) was diluted with a control (wild type, wt) sample (CN 2, screened by MLPA) to create "artifical mosaics" (CN 2.4, 2.3, 2,25, 2.2, 2.15, 2.1). Dilutions, as well as the undiluted heterozygous sample, and the control, were tested, hybridised with Agilent reference DNA.
2016-02-01 | GSE71355 | GEO
Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin. Identification of genomic p53 binding sites in HCT116 cells by ChIP-seq.
2014-11-21 | E-GEOD-58714 | biostudies-arrayexpress
Project description:SNCA protein product, a-synuclein, is widely renowned for its role in synaptogenesis and implication in both aging and Parkinson’s Disease (PD), but research efforts are still needed to elucidate its physiological functions and mechanisms of regulation. In this work, we aim to characterize SNCA-AS1, antisense transcript to the SNCA gene, and its implications in cellular processes. The overexpression of SNCA-AS1 upregulates both SNCA and a-synuclein, and through RNA-seq analysis we investigated the transcriptomic changes of which both genes are responsible. We highlight how they impact neurites extension and synapses’ biology, through specific molecular signatures. We report a reduced expression of markers associated with synaptic plasticity, and we specifically focus on GABAergic and dopaminergic synapses, for their relevance in aging processes and PD, respectively. A reduction in SNCA-AS1 expression leads to the opposite effect. As part of this signature is co-regulated by the two genes, we discriminate between functions elicited by genes specifically altered by SNCA-AS1 or SNCA’s overexpression, observing a relevant role for SNCA-AS1 in synaptogenesis through a shared molecular signature with SNCA. We also highlight how numerous deregulated pathways are implicated in aging-related processes, suggesting that SNCA-AS1 could be a key player in cellular senescence, with implications for aging-related diseases. Indeed, the upregulation of SNCA-AS1 leads to alterations in numerous PD specific genes, with an impact highly comparable to that of SNCA’s upregulation. Our results show that SNCA-AS1 elicits its cellular functions through the regulation of SNCA, with a specific modulation of synaptogenesis and senescence, presenting implications in PD.
2021-12-23 | GSE186255 | GEO