Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of P3HR-1 cells expressing control, smc1a, supt16h, med12, or tada2b sgRNAs and Akata EBV+ cells expressing control or myc sgRNAs

ABSTRACT: Transcriptome analysis of P3HR-1 cells expressing control, smc1a, supt16h, med12, or tada2b sgRNAs and Akata EBV+ cells expressing control or myc sgRNAs

PROVIDER: PRJNA590462 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis of P3HR-1 cells expressing control, smc1a, supt16h, med12, or tada2b sgRNAs and Akata EBV+ cells expressing control or myc sgRNAs

Project description:To gain insights into how EBV latency is maintained, we performed a human genome-wide CRISPR screen in latently EBV-infected Burkitt lymphoma B-cells. Our analyses identified a network of host factors that repress EBV lytic reactivation, centered on the transcription factor MYC and including cohesins, FACT, STAGA and Mediator. RNAseq was used to identify host and viral transcriptome changes in P3HR-1 Burkitt lymphoma cells expressing control, smc1a, supt16h, med12, or tada2b sgRNAs. RNAseq was used to identify host and viral transcriptome changes in Akata EBV+ burkitt lymphoma cells expressing control or myc sgRNAs.

2020-04-20 | GSE140651 | GEO

RNA-seq of CT26 cells expressing control or Gna13 targeting sgRNAs

Project description:CT26 cells expressing lentiviral Cas9 and sgRNAs targeting either control or Gna13

2021-10-01 | E-MTAB-10727 | biostudies-arrayexpress

RNA-seq of CT26 subcutaneous tumors expressing control or Gna13 targeting sgRNAs

Project description:CT26 cells expressing lentiviral Cas9 and sgRNAs targeting either control or Gna13 were transplanted into immunocompetent BALB/c mice. Tumors were harvested and processed for RNA-seq

2021-10-01 | E-MTAB-10737 | biostudies-arrayexpress

RNA-seq of CT26 cells expressing control or Gna13 targeting sgRNAs

Project description:RNA-seq of CT26 cells expressing control or Gna13 targeting sgRNAs

| PRJEB46347 | ENA

RNA-seq of CT26 subcutaneous tumors expressing control or Gna13 targeting sgRNAs

Project description:RNA-seq of CT26 subcutaneous tumors expressing control or Gna13 targeting sgRNAs

| PRJEB46348 | ENA

RNA-sequencing analysis of differential expression in supt16h mutants

Project description:Haematopoietic stem cells (HSCs) have long been the focus of developmental and regenerative studies, yet our understanding of the signalling events regulating their specification remains incomplete. We demonstrate that supt16h, a component of the FAcilitates Chromatin Transcription (FACT) complex, is required for HSC formation. Zebrafish supt16h mutants express reduced levels of Notch signalling components, genes essential for HSC development, due to abrogated transcription. Classically, Supt16h regulates transcription and nucleosome reorganization. Whereas global chromatin accessibility in supt16h mutants is unaffected, we observe a specific increase in accessibility at the p53 locus, causing an accumulation of p53 mRNA and protein. We further demonstrate that P53 levels directly influence expression of the Polycomb Group protein, phc1, which functions as a transcriptional repressor of Notch genes. Suppression of phc1 or its upstream regulator, p53, rescues both loss of Notch and loss of HSC phenotypes in supt16h mutants. Taken together, our results highlight a previously uncharacterized relationship between supt16h, p53, and phc1 to specify HSCs via modulation of Notch signalling.

2020-09-01 | GSE127555 | GEO

P53 based ChIP-sequencing of wildtype and mutant supt16h-/- zebrafish

Project description:Hematopoietic stem cells (HSCs) have long been the focus of developmental and regenerative studies, yet our understanding of the signaling events regulating their specification remains incomplete. We demonstrate that supt16h, a component of the FAcilitates Chromatin Transcription (FACT) complex, is required for HSC formation. Zebrafish supt16h mutants express reduced levels of Notch signaling components, genes essential for HSC development, due to abrogated transcription. Classically, Supt16h regulates transcription and nucleosome reorganization. Whereas global chromatin accessibility in supt16h mutants is unaffected, we observe a specific increase in accessibility at the p53 locus, causing an accumulation of p53 mRNA and protein. We further demonstrate that P53 levels directly influence expression of the Polycomb Group protein, phc1, which functions as a transcriptional repressor of Notch genes. Suppression of phc1 or its upstream regulator, p53, rescues both loss of Notch and loss of HSC phenotypes in supt16h mutants. Taken together, our results highlight a previously uncharacterized relationship between supt16h, p53, and phc1 to specify HSCs via modulation of Notch signaling.

2020-09-01 | GSE116088 | GEO

Gene expression data of human keratinocytes knocked down for SMC1A, SMC3, or control shRNA.

Project description:The purpose of the study is to understand the impacts of cohesin knockdown on epidermal gene expression. Primary human keratinocytes were knocked down for SMC1A, SMC3, or control to determine its genome-wide gene expression profile. Global gene expression profiling using U133 plus 2.0 arrays were used to deteremine the genes perturbed by knockdown of SMC1A or SMC3.

2017-11-15 | GSE83870 | GEO

Comparative chromatin accessibility profiling of wildtype and supt16h-/- zebrafish using ATAC-sequencing

Project description:Chromatin organization and accessibility are fundamental to how genes are transcriptionally controlled. We identify the first vertebrate mutant for supt16h, a component of the FACT (FAcilitates Chromatin Transcription) complex along with Ssrp1 known to reorganize nucleosomes and assist in transcriptional elongation. We demonstrate its importance in hematopoietic stem cell (HSC) specification by regulating the elongation of Notch genes. Unexpectedly, Assay for Transposase Accessible Chromatin (ATAC) sequencing revealed that loss of supt16h does not affect histone accessibility on a Notch-specific or global level. Although the majority of genes are unaffected, loss of supt16h alters chromatin accessibility significantly at the p53 locus, leading to its overexpression in mutants. Upon downregulation of p53, both loss of Notch and loss of HSC phenotypes are rescued. Notably, ssrp1 mutants possessed normal elongation of Notch genes, levels of P53, and specification of HSCs. Our results highlight the discrete effects of Supt16h and Ssrp1 during HSC specification. Additionally, we demonstrate the relationship between supt16h and p53 during transcriptional elongation to specify HSC fate via modulation of Notch signaling.

2020-09-01 | GSE106341 | GEO

SMC1A ChIP-seq in primary human keratinocytes

Project description:This study examines the DNA binding regions of SMC1A, a subunit of the Cohesin complex, in undifferentiated human keratinocytes.

2017-10-01 | GSE85526 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data