Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global poly(A+) RNA-seq profiling in control and CFIm25 KD human embryonic stem cells (H9 cell line)

ABSTRACT: To understand how CFIm25, an mRNA 3' processing regulator, affects the global poly(A+) RNAs profiling in hESCs (H9 cell line). We carried out poly(A+)-seq in control (2 samples) and CFIm25 KD (3 samples) hESCs.Using a cutoff value (P<0.05, fold change>1), in total, 577 differentially expressed genes (268 down-regulated genes and 309 up-regulated genes) were found upon CFIm25 KD, and the number of down-regulated genes and up-regulated genes were 84 and 128 respectively if using the cutoff value (P<0.05, fold change>2).

ORGANISM(S): Homo sapiens

PROVIDER: GSE176327 | GEO | 2022/04/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

poly(A+)-seq profiling of gene expression in control H9 and (CFIm25 KD+ 3Flag-CFIm25 overexpression) H9 cell lines

Project description:We carried out CFIm25 KD experiments in H9 cell line (hESCs). After poly(A+)-seq, we found the expression of hundreds of genes were changed. To investigate if the effect is a direct or indirect effect of CFIm25 KD, we next carried out 3Flag-CFIm25 overexpression in CFIm25 KD cells for gene-rescue experiments. After we obtained this cell line, here we performed poly(A+)-seq in control H9 and (CFIm25 KD+ 3Flag-CFIm25 overexpression)H9 cell lines. The goal of this experiment is to investigate if CFIm25 overexpression could rescue the gene expression phenotype caused by CFIm25 KD.

2022-04-21 | GSE176328 | GEO

Comparison of genomic binding profile for CFIm25 in control and CFIm25 KD hESCs (H9 cell line)

Project description:To understand how CFIm25 associates with genomic DNA during co-transcriptional mRNA processing,we carried out ChIP-seq analysis for CFIm25 in control and CFIm25 KD cells (CFIm25 KD cells as normalization background)

2022-04-21 | GSE178076 | GEO

Comparison of genomic binding profile for RNA polyII in control and CFIm25 KD hESCs (H9 cell line)

Project description:To understand how CFIm25 depletion affects gene expression at the transcription level, we carried out ChIP-seq analysis for RNAPII in control and CFIm25 KD cells.

2022-04-21 | GSE176543 | GEO

CFIm25 links alternative polyadenylation to glioblastoma tumour suppression

Project description:Purpose: To identify all of the APA targets of CFIm25 on a global scale and develop an algorithm that can idenitify APA events from standard RNA-seq data Methods: RNA from HeLa cells treated with control siRNA and CFIm25 siRNA were subject to RNA-Seq. Using a custom-designed algorithm to mine RNA-seq data for novel APA events regulated by CFIm25. Results: We identified over 1,400 genes with shortened 3’UTRs after CFIm25 knockdown. Importantly, we show that as a consequence of APA, many of these mRNAs have greatly enhanced protein expression due to the loss of destabilizing features within the 3’UTR. Conclusions: Our study underscored the critical function of the CFIm complex members in governing APA and establish a previously unknown link between APA and metabolic pathways important for tumor progression. Hela cell line mRNA profiles of control treated and CFIm25 Knockdown were generated by RNA-Seq using Illumina GAIIx.

2014-05-15 | E-GEOD-42420 | biostudies-arrayexpress

Comparison of genomic binding profile for several transcription factors and 3' processing factors in control and CFIm25 KD hESCs (H9 cell line)

Project description:To understand how CFIm25 depletion affects gene expression at the transcription level, we carried out ChIP-seq analysis for several transcription factors and 3' processing factors in control and CFIm25 KD cells.

2022-04-21 | GSE178075 | GEO

poly(A+)-seq profiling of gene expression in control H9 and (CFIm25 KD+ 3Flag-CFIm25 overexpression) H9 cell lines

Project description:poly(A+)-seq profiling of gene expression in control H9 and (CFIm25 KD+ 3Flag-CFIm25 overexpression) H9 cell lines

| PRJNA735770 | ENA

Partial loss of CFIm25 causes aberrant alternative polyadenylation and learning deficits

Project description:We previously showed that NUDT21-spanning copy-number variations (CNVs) are associated with intellectual disability (ID), and that NUDT21-encoded CFIm25 regulates the protein levels of at least one dose-sensitive, ID-associated protein: MeCP2 (Gennarino et al., 2015). However, the patients’ CNVs also spanned multiple other genes raising the possibility that loss or gain of these other genes caused their symptoms. To determine if reduced NUDT21 function alone is sufficient to cause disease, we generated Nudt21 heterozygous null mice to mimic the human state of reduced expression. We found that although these mice have 50% reduced Nudt21 mRNA, they only have 30% less of its cognate protein, CFIm25. Despite this partial protein-level compensation, the Nudt21+/- mice have learning deficits and cortical hyperexcitability. Further, to determine the molecular mechanism driving neural dysfunction, we partially inhibited NUDT21 in human embryonic stem cell-derived neurons to reduce CFIm25 by 30%. This reduction in CFIm25 was sufficient to induce misregulated alternative polyadenylation (APA) and protein levels in hundreds of genes, dozens of which are associated with intellectual disability and whose dysregulation is likely contributing to disease symptoms. Altogether, these results indicate that disruption of NUDT21-regulated APA events in the brain can cause intellectual disability.

2019-08-14 | PXD014842 | Pride

Global PAS-seq (polyA-site-sequencing) profiling in control and CFIm25 KD human embryonic stem cells (H9 cell line)

Project description:To understand how CFIm25, an mRNA 3' processing regulator, affects global mRNA alternative polyadenylation (APA) profiling in H9 cells. We performed PAS-seq (polyadenylation site sequencing) in control (2 samples) and CFIm25 KD cells (3 samples). PAS-seq library was prepared using a lexogen kit (3'-seq, Catolog. 016.024). Sequencing was performed using Novaseq PE150.

2022-04-21 | GSE176343 | GEO

CFIm25 links alternative polyadenylation to glioblastoma tumour suppression

2014-05-15 | GSE42420 | GEO

Knockdown of CFIm25 or CFIm68 decreases RNA polymerase II pausing and transcription

Project description:Transcription of eukaryotic protein-coding genes by RNA polymerase II (pol II) is highly regulated at initiation, elongation and termination and these steps are coordinated with co-transcriptional processing of the emerging pre-mRNA by capping, splicing, and cleavage and polyadenylation. Polyadenylation (Poly(A)) site recognition, which defines the end of the mRNA, relies on the cleavage and polyadenylation (CPA) complex. It was previously observed that knocking-down proteins of the CPA complex affects not only recognition of the poly(A) site but also results in increased pausing of pol II at the beginning of genes. This finding suggests that the CPA complex plays a role in regulating pol II turnover after transcription initiation. To explore this possibility, we knocked-down two subunits of the cleavage factor I (CFIm), CFIm25 and CFIm68, which are part of the CPA complex and involved in alternative polyadenylation, and performed pol II ChIP-seq. Surprisingly, we found that contrary to the effect of knocking down of other CPA factors, reduction of the level of CFIm25 or CFIm68 decreases pol II pausing and transcription genome-wide in HEK293 cells. These findings indicate that different subunits of the CPA complex have opposite effects on pol II pausing at the start of genes.

2019-06-20 | GSE99955 | 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