Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome-wide Profiling of N6‑Methyladenosine via a Selective Chemical Labeling Method

ABSTRACT: We present a chemical method (m6A-ORL-Seq) for transcriptome-wide m6A profiling , and compared its results with MeRIP-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185753 | GEO | 2021/10/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

Transcriptome-wide Profiling of N6‑Methyladenosine via a Selective Chemical Labeling Method

Project description:Transcriptome-wide Profiling of N6‑Methyladenosine via a Selective Chemical Labeling Method

| PRJNA770671 | ENA

Genome-wide identification of N6-methyladenosine by microarray

Project description:Although internal PolyA RNA modification N6-methyladenosine (m6A) plays essential roles in diverse biological processes, technology to detect precise m6A sites at transcriptome-wide scale is lacking. Here, we discovered that m6A interferes A (Adenine) – U (Uracil) or A-T (Thymidine) pairing. Based on differential hybridization between methylated vs. unmethylated RNAs to a DNA probe, we developed tiling microarray to pinpoint m6A sites in mouse transcriptome. We validated some of the identified sites and provided evidence to suggest that one functional mechanism of m6A is to block small RNA targeting to methylated mRNA. We designed a custom tiling array with to examine the precise location of m6A within meRIP-seq peaks from mouse embryonic stem cells determined in our previous publication (Wang et al., 2014). Each custom two-channel Agilent tiling array harbors 947,952 probes. Each probe is 25 nucleotides (nt), and any two adjacent probes in the genomic coordinate overlap each other by 19 nt. The Cy5 or red channel corresponds to Mettl14 knockout (M14) or DZA mutant mESC cell line, and Cy3 or green channel is associated with wild type cell line treated with scramble hairpin (SCR). Thus, in principle a higher Cy5/Cy3 signal for each probe reflects an increased hybridization to the oligonucleotide due to de-methylation of a particular RNA molecule in M14 or DZA condition relative to the SCR control. Moreover, we employed additional arrays with both channels dedicated for M14 as an external control for technical difference between the Cy5 and Cy3 dye (details below). For each comparison, we have three biological replicates, and therefore there are 9 tiling arrays in total (i.e., 3 arrays for M14 vs SCR, 3 arrays for DZA vs SCR, and 3 arrays for M14 vs M14).

2015-09-08 | E-GEOD-62530 | biostudies-arrayexpress

High-resolution transciptome mapping and N6-methyladenosine modification mapping of RAW264.7 cell lines treated with TCP, TBP or TIP.

Project description:Purpose:Detect transcriptome-wide mapping of m6A modifications by MeRIP-seq between normal and chemical-treated RAW264.7 cells. Methods:Total RNA was extracted using TRIzol Reagent followed by chemical fragmentation. The fragmented RNA was incubated with anti-m6A antibody. The desired m6A-enriched RNA eluate was used to construct cDNA library in parallel with input control. Conclusion: Our study revealed the difference of m6A-methylated RNA between normal and TCP/TBP/TIP-treated cells by RNA-seq and MeRIP-seq technologies.

2021-07-01 | GSE174678 | GEO

High-resolution transciptome mapping and N6-methyladenosine modification mapping of 3T3-L1 derived adipocytes

Project description:Purpose:Detect transcriptome-wide mapping of m6A modifications by MeRIP-seq between Rhein and DMSO treated 3T3-L1 differentiation adipocytes at the preadipocytes, MCE stage and differentiation stage. Methods:Total RNA was extracted using TRIzol Reagent followed by chemical fragmentation. The fragmented RNA was incubated with anti-m6A antibody. The desired m6A-enriched RNA eluate was used to construct cDNA library in parallel with input control. Conclusion: Our study revealed the difference of m6A-methylated RNA between DMSO and Rhein treated cells by RNA-seq and MeRIP-seq technologies.

2021-06-01 | GSE173702 | GEO

Antibody-free enzyme-assisted chemical approach for detection of N6-methyladenosine

Project description:We applied chemical-assisted, m6A-SEAL method to profile m6A distributions in the transcriptomes of human and plant cells and compared its results against MeRIPm6A-seq.

2020-04-22 | GSE129979 | GEO

High-resolution transcriptome mapping and N6-methyladenosine modification mapping of 3T3-L1 derived adipocytes (RNA-Seq)

2021-06-01 | GSE171785 | GEO

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

Transcriptome-wide N6-methyladenosine proﬁling of bovine skeletal myoblasts differentiation

Project description:We ascertain that mRNA m6A methylation exhibits declined change during bovine skeletal myoblast myogenic differentiation. RNA-seq and m6A-seq (MeRIP-seq) analysis reveal that m6A methylation is an abundant modification in the mRNA of bovine myoblast and myotubes, and the m6A sites are mainly enriched near the stop codons and the 3′ untranslated regions.

2021-12-29 | GSE173477 | GEO

Dynamic N6-methyladenosine Epitranscriptomic Landscape in Lung Adenocarcinoma

Project description:Systematically evaluate the global effect of dysregulated m6A regulators on the m6A epitranscriptome in patient tumors, and identify prognostic m6A markers by linking with patients' clinicopathological and outcome information.

| EGAS00001005524 | EGA

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