Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LOX-1 is an N6-methyladenosine-regulated receptor for Helicobacter pylori via binding to the bacterial catalase [RNA-seq]

ABSTRACT: The role of N6-methyladenosine (m6A) modification of host mRNA during bacterial infection is unclear. Here, we show that Helicobacter pylori infection upregulated major m6A “writers” and increased m6A level in gastric epithelial cells. Attenuating m6A increase by hemizygotic deletion of Mettl3 in mice or small interfering RNAs targeting m6A “writers” exacerbated H. pylori colonization. LOX-1 mRNA was identified as a key m6A-regulated target during H. pylori infection. m6A modification destabilized LOX-1 mRNA and reduced LOX-1 protein level. LOX-1 acted as a membrane receptor for H. pylori catalase to mediate the bacterial adhesion. BI-0115, a small-molecule inhibitor of LOX-1, suppressed H. pylori adhesion and colonization. Genetic ablation of Lox-1 also reduced H. pylori colonization in mice. In sum, this study reveals that m6A modification is an auto-protective mechanism against H. pylori infection by downregulating LOX-1 to prevent H. pylori adhesion. LOX-1 could be a druggable target for controlling H. pylori infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE220721 | GEO | 2022/12/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

LOX-1 is an N6-methyladenosine-regulated receptor for Helicobacter pylori via binding to the bacterial catalase [m6A-seq]

Project description:The role of N6-methyladenosine (m6A) modification of host mRNA during bacterial infection is unclear. Here, we show that Helicobacter pylori infection upregulated major m6A “writers” and increased m6A level in gastric epithelial cells. Attenuating m6A increase by hemizygotic deletion of Mettl3 in mice or small interfering RNAs targeting m6A “writers” exacerbated H. pylori colonization. LOX-1 mRNA was identified as a key m6A-regulated target during H. pylori infection. m6A modification destabilized LOX-1 mRNA and reduced LOX-1 protein level. LOX-1 acted as a membrane receptor for H. pylori catalase to mediate the bacterial adhesion. BI-0115, a small-molecule inhibitor of LOX-1, suppressed H. pylori adhesion and colonization. Genetic ablation of Lox-1 also reduced H. pylori colonization in mice. In sum, this study reveals that m6A modification is an auto-protective mechanism against H. pylori infection by downregulating LOX-1 to prevent H. pylori adhesion. LOX-1 could be a druggable target for controlling H. pylori infection.

2022-12-11 | GSE220541 | GEO

m6A sequencing of HIV viral genomic RNA and infected host cell samples

Project description:The internal N6-methyladenosine (m6A) methylation of eukaryotic nuclear RNA controls post-transcriptional gene expression, which is regulated by methyltransferases (writers), demethylases (erasers), and m6A-binding proteins (readers) in cells. The YTH domain family proteins (YTHDF1–3) bind to m6A-modified cellular RNAs and affect RNA metabolism and processing. Here, we show that YTHDF1–3 proteins recognize m6A-modified HIV-1 RNA and inhibit HIV-1 infection in cell lines and primary CD4+ T-cells. We further mapped the YTHDF1–3 binding sites in HIV-1 RNA from infected cells. We found that the overexpression of YTHDF proteins in cells inhibited HIV-1 infection mainly by decreasing HIV-1 reverse transcription, while knockdown of YTHDF1–3 in cells had the opposite effects. Moreover, silencing the m6A writers decreased HIV-1 Gag protein expression in virus-producing cells, while silencing the m6A erasers increased Gag expression. Our findings suggest an important role of m6A modification of HIV-1 RNA in viral infection and HIV-1 protein synthesis.

2016-08-18 | GSE85724 | GEO

Transcriptome-wide mapping of host mRNA m6A modification to decipher the role of gut microbiome

Project description:A recently layer of gene expression regulation is N6-methyladenosine (m6A) mRNA modification. The role of gut microbiota in modulating host m6A epitranscriptomic and gene expression has not been studied. To decipher the role of gut microbiome, we profiled m6A mRNA modification epitranscriptomic mark in conventional mice compared to germ free mice. Transcriptome-wide mapping of host m6A mRNA modifications in four mice tissues allowed us to discover that gut microbiota can greatly impact host m6A mRNA modifications. The expression levels of m6A writers in mice tissues are regulated by gut microbiota. In conclusion, we report transcriptome-wide mapping of host m6A mRNA modifications regulated by gut microbiota. The present study can help better understand the role of the microbiome in host gene expression and host-microbiome interactions.

2018-12-28 | GSE120262 | GEO

Transcriptome profiling of m6A mRNA modification in GES-1 cells infected by Helicobacter pylori

Project description:Helicobacter pylori (H.pylori) infection is an important factor in the occurrence of human gastric diseases, but its pathogenic mechanism is not clear. N6-methyladenosine (m6A) is the most prevalent reversible methylation modification in mammalian RNA and it plays a crucial role in controlling many biological processes. We used MeRIP-seq technology to sequence the GES-1 cells infected with Helicobacter pylori(H. pylori) for 48 h.

2023-05-11 | GSE230869 | GEO

Transcriptome-wide N6-methyladenosine modification profiling of mRNAs during infection of Newcastle disease virus in Chicken Macrophages

Project description:N6-methyladenosine (m6A) modification is the most prevalent post-transcriptional modification of mRNA in eukaryotes and has been reported to play an important role in viral infection. However, the role of m6A modification during Newcastle disease virus infection (NDV) is not clear. In this study, we profiled the transcriptome-wide m6A modification of mRNA in NDV-infected chicken macrophages using MeRIP-seq. we identified a total of 9496 significantly changed peaks, of which 7015 peaks distributed across 3320 genes were significantly up-regulated and 2481 peaks distributed across 1264 genes were significantly down-regulated. Combined analysis of m6A peaks and mRNA expression revealed 1234 mRNAs with significantly altered methylation and expression levels after NDV infection, and m6A modification tended to have a negatively correlation with mRNA expression, suggesting that m6A modification may regulate the process of NDV infection by regulating gene expression, especially innate immunity-related genes. To our knowledge, This is the first comprehensive characterization of m6A patterns of the mRNA in chicken macrophages after NDV infection, and provides a valuable basis for further exploring the role of m6A modification in the process of NDV infection.

2023-05-24 | GSE208230 | GEO

Co-effects of m6A dynamics and chromatin accessibility changes regulate cardiomyocyte differentiation

Project description:The growth and differentiation of cardiomyocytes are primarily driven by gene expression dynamics, with various epigenetic modifications playing a crucial role in this process. One of the most common modifications on mRNA, m6A, influences the regulation of mRNA metabolism; however, its function remains enigmatic. In this study, we identified a correlation between m6A modification and cardiomyocyte differentiation by profiling m6A dynamics during the transition of pluripotent stem cells into cardiomyocytes. Although the overall m6A modification level remains relatively stable, most genes exhibit changes in their m6A levels as cardiomyocyte differentiation progresses. We observed that alterations in chromatin accessibility can impact the binding capabilities of m6A writers, erasers, and readers, consequently affecting m6A levels. Furthermore, the coordinated changes of m6A and chromatin accessibility are closely associated with early-stage cardiomyocyte differentiation. These findings suggest that m6A is a significant factor in determining the fate of cardiomyocyte differentiation, shedding light on its role in this critical process.

2023-08-24 | GSE231549 | GEO

Helicobacter pylori-induced changes in miRNA expression in human gastric epithelial cells

Project description:H. pylori infection of human gastric epithelial cells (GEC) represses H,K-ATPase alpha subunit (HK-alpha) gene transcription through NF-Kappa B p50 homodimer binding to HK-alpha promoter. The bacterial cagA and slt gene products have been implicated in HK-alpha repression, which facilitates gastric H. pylori colonization and may underlie transient clinical hypochlorhydria. We hypothesized that H. pylori also regulates H,K-ATPase expression post-transcriptionally by micro-RNA interaction with HK-alpha mRNA. Our microarray experiment examined the effect of infection by wildtype H. pylori infection or a delta-cagA H. pylori mutant on miRNA expression of human gastric cells (AGS). Our results indicate that H. pylori infection up-regulates GEC miRNAs that target the HK-alpha 3' UTR and block translation, and that CagA activity is implicated in the miRNA up-regulation.

2016-01-18 | GSE51306 | GEO

Identification of Helicobacter pylori genes contributing to stomach colonization.

Project description:Chronic infection of the human stomach with Helicobacter pylori leads to a variety of pathologic sequelae including peptic ulcer and gastric cancer, resulting in significant human morbidity and mortality. Several genes have been implicated in disease related to H. pylori infection including the vacuolating cytotoxin and the cag pathogenicity island. Other factors important for establishment and maintenance of infection include urease enzyme production, motility, iron uptake and stress response. We utilized a C57BL/6 mouse infection model to query a collection of 2400 transposon mutants in two different bacterial strain backgrounds for H. pylori genetic loci contributing to colonization of the stomach. Microarray based tracking of transposon mutants allowed us to monitor the behavior of transposon insertions in 758 different gene loci. Of the loci measured 223 (29%) had a predicted colonization defect. These include previously described H. pylori virulence genes, genes implicated in virulence in other pathogenic bacteria and 81 hypothetical proteins. We have retested 10 previously uncharacterized candidate colonization gene loci by making independent null alleles and confirmed their colonization phenotype using competition experiments and determination of the dose required for 50% infection. Of the genetic loci retested, 60% have strain specific colonization defects while 40% had phenotypes in both strain backgrounds for infection, highlighting the profound effect of H. pylori strain variation on the pathogenic potential of this organism. This SuperSeries is composed of the SubSeries listed below.

2006-12-15 | GSE6531 | GEO

Effect of Heat stress on m6A modification in CaSki cell

Project description:N6-methyladenosine (m6A) occurs extensively on multiple RNA species and is the most abundant internal modification of eukaryotic messenger RNA (mRNA). RNA m6A methylation is a dynamic and reversible process subjected to regulation by three categories of m6A modifier proteins, including m6A methyltransferases/writers (e.g., METTL3/14 methyltransferase complex and METTL16), m6A demethylases/erasers (e.g., FTO and ALKBH5) and m6A binding proteins/readers (e.g., YTH family proteins and IGF2BPs). The dynamic and adjustable nature makes m6A a key regulator in RNA metabolism, and the fate of m6A-modified RNA is modulated by m6A readers. Previous studies have demonstrated that fever can benefit survival of cancer patients, and currently hyperthermia (elevating body temperature beyond normal) is either administered alone or in combination with radiotherapy or chemotherapy to treat various neoplasms with unclear mechanisms. Accruing evidence has revealed favorable effects of fever/hyperthermia in cancer treatment through affecting the properties of oncogenic proteins (e.g., stability, posttranslational modification, ability to interact with other molecules). Accordingly, we sought to investigate whether and how heat stress affects cancer development by m6A modification.

2022-02-25 | GSE197247 | GEO

Transcriptome-wide regulation of host m6A mRNA methylation by malaria parasite infection

Project description:N6-Methyladenosine (m6A) modification has been found to play important roles in diverse pathogen infections and host responses, here we report host m6A mRNA transcriptome profiles regulated by the infections of two strains of malaria parasite Plasmodium yoelii (N67 and N67C). We showed that malaria infection can regulate host m6A mRNA modification and reprogram host m6A mRNA methylome by mediating corresponding m6A catalytic enzyme levels. Our data suggested m6A modification as a significant transcriptome-wide mark during host-malaria interactions.

2021-05-24 | GSE150546 | 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