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ABSTRACT: Study of the RNA splicing in METTL4 knockout HeLa S3 cells

PROVIDER: PRJNA1162735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30719213.fastq.gz	Fastqsanger.gz
	SRR30719214.fastq.gz	Fastqsanger.gz
	SRR30719215.fastq.gz	Fastqsanger.gz
	SRR30719216.fastq.gz	Fastqsanger.gz
	SRR30719217.fastq.gz	Fastqsanger.gz

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Project description:Study of the RNA splicing in THUMPD2 knockout HeLa S3 cells

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Mettl4 limits the proliferation and differentiation of neural stem cells via regulating RNA alternative splicing

Project description:Previous studies indicate that Mettl4 regulates gene expression and RNA splicing. However, the biological functions of METTL4 remain unclear. Here we show that the absence of Mettl4 leads to sub lethality in mouse and promotes brain function in processing learning and working memory. The neural stem cells in subgranular zone are more proliferative in Mettl4 knockout mice compared with wild type mice. The proliferation and neurogenesis of primary neural stem cells are increased in the absence of Mettl4. Meanwhile, Mettl4 knockout NSCs are more sensitive low levels of H2O2, which is known to promote proliferation and neurogenesis of neural stem cells. The biological effects caused could be due to the altered gene expression or alternative splicing in neural stem cells when Mettl4 is absent. To investigate the effects at transcriptome level, we performed RNA sequencing.

2023-09-30 | GSE212821 | GEO

Project description:Study of the splicing in Mettl4 knockout mice

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STAT1 transcription factor in Human HeLa S3

Project description:We report the results of chromatin immunoprecipitation following by high-thoughput tag sequencing (ChIP-Seq) using the GA II platform from Illumina for the human transcription factor STAT1 in HeLa S3 cells. The STAT1 ChIP was performed using HeLa S3 cells that are stimulated using gamma-interferon. We have also generated a seqenced input DNA dataset for gamma-interferon stimulated HeLa S3 cells. Raw data for this study is available for download from the Short Read Archive database at: http://www.ncbi.nlm.nih.gov/Traces/sra/sra.cgi?study=SRP000703. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

2008-09-16 | GSE12782 | GEO

Overlapping Splicing Regulatory Networks of the Nuclear Matrix Protein Matrin3 and PTB

Project description:Transcription and alternative splicing profiling in control and Matr3 siRNA treated HeLa S3 cells.

2014-11-27 | E-MTAB-3092 | biostudies-arrayexpress

STAT1 transcription factor in Human HeLa S3

2008-09-15 | E-GEOD-12782 | biostudies-arrayexpress

METTL4 catalyzes m6Am methylation in U2 snRNA to regulate pre-mRNA splicing

Project description:N6-methylation of 2’-O-methyladenosine (Am) in RNA occurs in eukaryotic cells to generate N6,2’-O-dimethyladenosine (m6Am). Identification of the methyltransferase responsible for m6Am catalysis has accelerated studies on the function of m6Am in RNA processing. While m6Am is generally found in the first transcribed nucleotide of mRNAs, the modification is also found internally within U2 snRNA. However, the writer required for catalyzing internal m6Am formation had remained elusive. By sequencing transcriptome-wide RNA methylation at single-base-resolution, we identified human METTL4 as the writer that directly methylates Am at U2 snRNA position 30 into m6Am. We found that METTL4 localizes to the nucleus and its conserved methyltransferase catalytic site is required for U2 snRNA methylation. By sequencing human cells with overexpressed Mettl4, we determined METTL4’s in vivo target RNA motif specificity. In the absence of Mettl4 in human cells, U2 snRNA lacks m6Am thereby affecting a subset of splicing events that exhibit specific features such as overall 3’ splice-site weakness with certain motif positions more affected than others. This study establishes that METTL4 methylation of U2 snRNA regulates splicing of specific pre-mRNA transcripts.

2020-08-17 | GSE144745 | GEO

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Project description:RNA-seq analysis of TALEN-mediated LATS2 knockout HeLa-S3 cells

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Genome-wide maps of CTCF and BHLHe40 binding in HeLa-S3 cells

Project description:In this study, we investigated CTCF and BHLHE40 binding in HeLa-S3 cells transfected with control shRNA and specific shRNA.

2020-08-14 | GSE137848 | GEO

CTCF regulates positioning of the human cystic fibrosis gene in association with a histone deacetylase

Project description:Treatment with the histone deacetylase inhibitor trichostatin a (TSA) changes the radial positioning of the CFTR gene in HeLa S3 cells. The gene relocates from the nuclear periphery to the nuclear interior. In Calu-3 cells the gene is located in the nuclear interior. To identifiy potential regulatory elements for the positioning of CFTR, the histone h3 and h4 acetylation patterns of untreated and TSA-treated HeLa S3 and untreated Calu-3 cells were determined by ChIP-chip. A CTCF site close to the CFTR promoter displayed consistent histone H3 hyperacetylation in TSA treated HeLa S3 cells and Calu-3 cells.

2013-12-31 | GSE29360 | GEO

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