Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-nucleotide resolution profiling of N6-methyladenosine in SETD2 knockdown HepG2 cells [m6A miCLIP-seq]

ABSTRACT: Single-nucleotide resolution profiling of N6-methyladenosine in SETD2 knockdown HepG2 cells [m6A miCLIP-seq]

PROVIDER: PRJNA499111 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Single-nucleotide resolution profiling of N6-methyladenosine in SETD2 knockdown HepG2 cells [m6A miCLIP-seq]

Project description:To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 knockdown and control HepG2 cells by miCLIP-seq, and found the depletion of H3K36me3 by SETD2 silencing globally reduced m6A in the human transcriptome.

2019-02-21 | GSE121942 | GEO

Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

Project description:Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

| PRJNA433472 | ENA

Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

Project description:SETD2 is the specific methyltransferase of H3K36me3, while METTL3, METTL14 and WTAP are the components of m6A methyltransferase complex. To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 and METTL3, METTL14 or WTAP knockdown HepG2 cells, and found depletion of H3K36me3 by SETD2 silencing globally reduced m6A in human transcriptome. What’s more, most of the SETD2-dependent hypomethylation sites also responded to knockdown of METTL3, METTL14, or WTAP.

2019-02-21 | GSE110320 | GEO

Profiling of N6-methyladenosine in mouse embryonic stem cells: Setd2 knockdown and control cells

Project description:Profiling of N6-methyladenosine in mouse embryonic stem cells: Setd2 knockdown and control cells

| PRJNA433611 | ENA

N6-Methyladenosine methylation profile in rat H9C2 cardiomyocytes under the hypoxic stress

Project description:Hypoxia as a crucial pathogenesis factor usually results in huge harmful effects on cardiac injury and dysfunction. In our previous study (PMID: 33294289), We observe a series of differential expressed genes between transcription and translation, which may be attributed to the hypoxia-specific binding affinity of Nuclear cap-binding subunit 3 (NCBP3) at 5’ un-translation region of target genes. But the underlying molecular mechanism of NCBP3 for gene translation modulation remains unclear. Here, we conducted RIP-seq of N6-Methyladenosine methylation in H9C2 cells with the conditions of normoxic, hypoxic and with additional NCBP3 knockdown.

2021-06-30 | E-MTAB-10682 | biostudies-arrayexpress

N6-methyladenosine Modulates Messenger RNA Translation Efficiency

Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

2015-06-09 | E-GEOD-63591 | biostudies-arrayexpress

YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RIP-seq dataset

Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.

2022-02-04 | E-MTAB-11321 | biostudies-arrayexpress

FMRP facilitates the nuclear export of N6-methyladenosine-containing mRNAs

Project description:FMRP facilitates the nuclear export of N6-methyladenosine-containing mRNAs.

2019-11-21 | GSE133724 | GEO

Widespread N6-methyladenosine-dependent RNA Structural Switches Regulate RNA-Protein Interactions

Project description:We show that N6-methyladenosine (m6A), the most abundant internal modification in mRNA/lncRNA with still poorly characterized function, alters RNA structure to facilitate the access of RBM for heterogeneous nuclear ribonucleoprotein C (hnRNP C). We term this mechanism m6A-switch. Through combining PAR-CLIP with Me-RIP, we identify 39,060 m6A-switches among hnRNP C binding sites transcriptome-wide. We show that m6A-methyltransferases METTL3 or METTL14 knockdown decreases hnRNP C binding at 16,582 m6A-switches. Taken together, 2,798 m6A-switches of high confidence are identified to mediate RNA-hnRNP C interactions and affect diverse biological processes including cell cycle regulation. These findings reveal the biological importance of m6A and provide insights into the sophisticated regulation of RNA-RBP interactions through m6A-induced RNA structural remodeling. Measure the m6A methylated hnRNP C binding sites transcriptome-wide by PARCLIP-MeRIP; measure the differential hnRNP C occupancies upon METTL3/METTL14 knockdown by PAR-CLIP; measure RNA abundance and splicing level changes upon HNRNPC, METTL3 and METTL14 knockdown

2015-02-27 | E-GEOD-56010 | biostudies-arrayexpress

Profiling of N6-methyladenosine in mouse embryonic stem cells: Setd2 knockdown and control cells

Project description:Setd2 is the specific methyltransferase of H3K36me3. To understand the global effect of H3K36me3 on m6A modification, we used mouse embryonic stem cells (mESCs) model with doxycycline (Dox)-induced Setd2 knockdown, and performed m6A-IP followed by sequencing in mESCs with or without Dox treatment. We found that depletion of H3K36me3 by Setd2 silencing globally reduced m6A in mouse transcriptome.

2019-02-21 | GSE110322 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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