Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Toe1 konckout Transcriptomes in undifferentiated C17.2 cells

ABSTRACT: We extracted RNA from KO-NC and KO-Toe1 undifferentiated C17.2 cells for high-throughput transcriptomic sequencing.In undifferentiated C17.2 cells, Toe1 primarily influenced key biological processes such as calcium ion binding, the extracellular matrix (ECM), and alpha-amino acid catabolism

ORGANISM(S): Mus musculus

PROVIDER: GSE254608 | GEO | 2024/11/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Toe1 konckout Transcriptomes in differentiated C17.2 cells

Project description:We extracted RNA from NC and KO-Toe1 differentiated C17.2 cells for high-throughput transcriptomic sequencing. In differentiated C17.2 cells, Toe1 primarily affected biological functions including peptidase activity, chemotactic factors, the ECM, and the TNF signaling pathway.

2024-11-13 | GSE254609 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Toe1 konckout Transcriptomes in undifferentiated C17.2 cells

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Toe1 konckout Transcriptomes in undifferentiated C17.2 cells

| PRJNA1071134 | ENA

Expression data from C17.2 progenitor cells during neural differentiation for 5 and 10 days with NGF and BDNF

Project description:We used microarray to study the change in gene expression during differentiation in the C17.2 progenitor cell line. The cells were either undifferentiated or differentiated for 5 or 10 days. The goal was to identify genes important for differentiation of the C17.2 cell line

2017-04-04 | GSE97337 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Toe1 konckout Transcriptomes in differentiated C17.2 cells

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Toe1 konckout Transcriptomes in differentiated C17.2 cells

| PRJNA1071133 | ENA

PARN and TOE1 constitute a 3′ end maturation module for nuclear non-coding RNAs

Project description:Poly(A)-specific ribonuclease (PARN) and target of EGR1 protein 1 (TOE1) are nuclear granule-associated deadenylases, whose mutations are linked to multiple human diseases. Here, we applied mTAIL-seq and RNA sequencing (RNA-seq) to systematically identify the substrates of PARN and TOE1 and elucidate their molecular functions. We found that PARN and TOE1 do not modulate the length of mRNA poly(A) tails. Rather, they promote the maturation of nuclear small non-coding RNAs (ncRNAs). PARN and TOE1 act redundantly on some ncRNAs, most prominently small Cajal body-specific RNAs (scaRNAs). scaRNAs are strongly downregulated when PARN and TOE1 are compromised together, leading to defects in small nuclear RNA (snRNA) pseudouridylation. They also function redundantly in the biogenesis of telomerase RNA component (TERC), which shares sequence motifs found in H/ACA box scaRNAs. Our findings extend the knowledge of nuclear ncRNA biogenesis, and they provide insights into the pathology of PARN/TOE1-associated genetic disorders whose therapeutic treatments are currently unavailable.

2018-03-30 | GSE111511 | GEO

The 3' exonuclease TOE1 selectively processes snRNAs through recognition of Sm complex assembly and 5’ cap trimethylation [global seq]

Project description:Competing exonucleases that promote 3’ end maturation or degradation direct quality control of small non-coding RNAs, but how these enzymes distinguish normal from aberrant RNAs is poorly understood. The Pontocerebellar Hypoplasia 7 (PCH7)-associated 3’ exonuclease TOE1 promotes maturation of canonical small nuclear RNAs (snRNAs). Here, we demonstrate that TOE1 achieves specificity towards canonical snRNAs by recognizing Sm complex assembly and cap trimethylation, two features that distinguish snRNAs undergoing correct biogenesis from other small non-coding RNAs. Indeed, disruption of Sm complex assembly via snRNA mutations or protein depletions obstructs snRNA processing by TOE1, and in vitro snRNA processing by TOE1 is stimulated by a trimethylated cap. An unstable snRNA variant that normally fails to undergo maturation becomes fully processed by TOE1 when its degenerate Sm binding motif is converted into a canonical one. Our findings uncover the molecular basis for how TOE1 distinguishes snRNAs from other small non-coding RNAs and explain how TOE1 promotes maturation specifically of canonical snRNAs undergoing proper processing.

2023-09-06 | GSE240773 | GEO

The 3' exonuclease TOE1 selectively processes snRNAs through recognition of Sm complex assembly and 5’ cap trimethylation [gene specific seq]

2023-09-06 | GSE240772 | GEO

The effect of berberine upon AAPH-damaged C17.2 neural stem cells

Project description:Berberine shows protective effect against AAPH-damaged C17.2 neural stem cells. This study aims to determine the genes regulated by berberine and clarify the possible molecular mechanism underlying the action.

2024-01-08 | GSE164469 | GEO

Biallelic mutations in the 3’ exonuclease TOE1 cause Pontocerebellar Hypoplasia Type 7 and result in snRNA processing defects

Project description:Processing of RNA polymerase II-transcribed spliceosomal small nuclear RNAs (snRNAs) initiates with cleavage by the Integrator complex, but the factors that subsequently remove 3’ end extensions from metazoan snRNAs have remained unknown. We studied human families with a unique recessive syndromic constellation of pontocerebellar atrophy with ambiguous genitalia, uncovering biallelic inactivating mutations in TOE1, which encodes a conserved unconventional deadenylase. TOE1 demonstrated tight association with snRNA-protein (snRNP) complexes with specificity for incompletely processed pre-snRNAs containing 3’ end extensions that often included post-transcriptionally added tails. Human cells deficient for TOE1 catalytic activity showed accumulation of 3’-end extended U1, U2, U4 and U5 pre-snRNAs, and TOE1 immuno-isolated from human cells was capable of processing 3’-end extended snRNPs in vitro. The missense mutations identified in patients impaired TOE1 stability and snRNA processing in patient cells, which was associated with defects in splicing. Our findings reveal the cause of a unique brain malformation and uncover a long-sought 3’ exonuclease required for snRNA processing.

2016-12-31 | GSE71536 | GEO

11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma.

Project description:High-risk 11q deleted neuroblastomas (NBs) typically display an undifferentiated/poorly differentiated morphology. NB is thought to develop from Schwann cell precursors (SCPs) and un-differentiated neural crest derived cells (NCC). It is therefore vital to understand the mechanisms involved in the block of differentiation. We showed that an important and novel role for oncogenic ALK-ERK1/2-SP1 signaling may be the maintenance of an undifferentiated state of transformed NC-derived progenitors that is achieved by repression of DLG2, a tumor suppressor in NB. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors (SCP) become chromaffin cells of the adrenal gland. The importance of SP1 and DLG2 in this process is highlighted by our findings that restoring DLG2 expression spontaneously drives NB differentiation. Further, genetic analysis of high-risk 11q deletion NB patient identified genetic lesions in the DLG2 gene, Our data also suggest that further exploration of other ‘bridge genes’ may help to better understand the mechanisms underlying the differentiation of NC-derived progenitors and their contribution to NB.

2020-11-25 | PXD017946 | Pride

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