Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome binding/occupancy profiling of ALKBH5 by high throughput sequencing [Cut&Tag]

ABSTRACT: Alkylation repair homolog protein 5 (ALKBH5) binds to RNA and mediates RNA m6A demethylation. However, whether ALKBH5 binds to DNA is largely unknown. In this study, our CUT&Tag assay identified 12333 peaks in ALKBH5-overexpressing Hepa1-6 cells, indicating that ALKBH5 can bind to DNA.

ORGANISM(S): Mus musculus

PROVIDER: GSE248568 | GEO | 2025/02/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome binding/occupancy profiling of ALKBH5 by high throughput sequencing [CUT&RUN]

Project description:Alkylation repair homolog protein 5 (ALKBH5) binds to RNA and mediates RNA m6A demethylation. However, whether ALKBH5 binds to DNA is largely unknown. In this study, our CUT&RUN data show that ALKBH5 can bind to DNA in Hepa1-6 cells.

2025-02-27 | GSE277052 | GEO

Genome binding/occupancy profiling of ALKBH5 by high throughput sequencing [Cut&Tag]

Project description:Genome binding/occupancy profiling of ALKBH5 by high throughput sequencing [Cut&Tag]

| PRJNA1044792 | ENA

ALKBH5 is a New Mammalian RNA Demethylase

Project description:N6-methyladenosine (m6A) is the most prevalent internal modification of messenger RNA (mRNA) in higher eukaryotes. Here we report ALKBH5 as a new mammalian demethylase that oxidatively removes the m6A modification in mRNA in vitro and inside cells. This demethylation activity of ALKBH5 significantly affects mRNA export and RNA metabolism as well as the assembly of mRNA processing factors in nuclear speckles. Alkbh5-deficient male mice are characterized by impaired fertility resulting from apoptosis that affects meiotic metaphase-stage spermatocytes. In accordance with this defect, we have identified in mouse testes 1552 differentially expressed genes which cover broad functional categories and include spermatogenesis-related mRNAs involved in the p53 functional interaction network. We show that Alkbh5-deficiency impacts the expression levels of some of these mRNAs, supporting the observed phenotype. The discovery of this new RNA demethylase strongly suggests that the reversible m6A modification plays fundamental and broad functions in mammalian cells. RNA-seq in two cell types

2013-02-15 | E-GEOD-40132 | biostudies-arrayexpress

ALKBH5

Project description:ALKBH5

| PRJNA932008 | ENA

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [CUT&Tag]

Project description:N6-methyladenonsine (m6A) modification locates ubiquitously in mammalian mRNA, and profoundly impacts various physiological processes and pathogenesis. However, the precise involvement of m6A in early endoderm development has yet to be fully elucidated. Here, we reported that depletion of the m6A demethylase ALKBH5 in human embryonic stem cells (hESCs) severely impaired definitive endoderm (DE) differentiation. Within this process, ALKBH5-/- hESCs failed to undergo the primitive streak (PS) intermediate transition, which is considered as a prelude to endoderm specification. Mechanistically, we demonstrated that ALKBH5 deficiency induced m6A hypermethylation around the 3’ untranslated region (3’UTR) of GATA6 transcripts and destabilized GATA6 mRNA in a YTHDF2-dependent manner. Moreover, dysregulation of GATA6 expression ablated its occupancy with critical regulators of Wnt/β-catenin signaling pathway, thereby disrupting the signaling logic underlying DE formation. Overall, our findings unveil a mechanism whereby the ALKBH5-GATA6-WNT/β-catenin axis modulates human in vitro DE induction, and present novel insights on m6A modification in early embryonic development.

2024-10-23 | GSE248527 | GEO

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [CUT&Tag]

Project description:ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [CUT&Tag]

| PRJNA1044428 | ENA

Essential role of ALKBH5-mediated RNA demethylation modification in bile acid-induced gastric intestinal metaplasia

Project description:Reflux of bile acids and subsequent caudal-related homeobox 2 (CDX2) activation contribute to gastric intestinal metaplasia (IM), which is a precursor of gastric cancer. However, the underlying mechanism by which bile acids cause this is not entirely clear. Here we demonstrated that alkylation repair homolog protein 5 (ALKBH5), which is a major RNA N6-adenosine demethylase, was required for bile acid-induced gastric IM. Mechanistically, we revealed the N6-methyladenosine (m6A) modification profile in gastric IM for the first time and identified ZNF333 as a bona fide m6A target of ALKBH5. ALKBH5 was shown to demethylate ZNF333 mRNA, leading to enhanced ZNF333 expression by abolishing m6A-YTHDF2-dependent mRNA degradation. In addition, ALKBH5 activated CDX2 and downstream intestinal markers by targeting the ZNF333/CYLD axis and activating NF-κB signaling. Reciprocally, p65, which is the key transcription factor of the canonical NF-κB pathway, enhanced the transcription activity of ALKBH5 in the nucleus, thus forming a positive feed-forward circuit. In addition, ALKBH5 levels were positively correlated with ZNF333 and CDX2 in IM tissues, indicating a significant clinical relevance. Collectively, our findings suggest an m6A modification-associated positive feed-forward loop between ALKBH5 and NF-κB signaling is involved in the generation of the IM phenotype from gastric epithelial cells. Targeting the ALKBH5/ZNF333/CYLD/CDX2 axis might be a useful therapeutic strategy for gastric IM in patients with bile regurgitation.

2021-10-14 | GSE179185 | GEO

Epigenome analysis of ALKBH5 knocked down HCT116 cell

Project description:ALKBH5 is one of the important m6A demethylases and is reported to be closely associated with tumorigenesis.In this study, we investigated whether ALKBH5 could affect genome-wide DNA methylation pattern. We investigated DNA methylation profile of ALKBH5 deleted HCT116 cell with control cell. The Illumina Infinium HumanMethylation 850K BeadChip was used. Samples included 2 HCT1116 shNC and 4 HCT116 shALKBH5.

2024-12-07 | GSE190375 | GEO

ALKBH5 is a New Mammalian Nuclear RNA Demethylase that Affects RNA Metabolism

Project description:To identify ALKBH5-binding RNA, PAR-CLIP was performed to pull down ALKBH5-binding RNAs. After digestion with Rnase T1, small RNA-seq was performed. Through analysis of 50 million reads, we have found 933 ALKBH5-binding genes, among which mRNA accounts for 85%. further analysis revealed that ALKBH5 mainly binds to intron and exon region of mRNAs. among 933 genes,64 genes have been reported to be spermatogenesis related, and most of them are functionally related with p53 signaling. we have also found 9 consensus binding motifs based on the clusters significantly detected in RIP sample.

2015-06-01 | GSE38482 | GEO

The m6A Demethylase ALKBH5 Maintains Tumorigenicity of Glioblastoma Stem-Like Cells by Sustaining FOXM1 Expression and Cell Proliferation Programing

Project description:The dynamic and reversible N6-methyladenosine (m6A) RNA modification installed and erased by N6-methyltransferases and demethylases regulates gene expression and cell fate. Here, we show that the m6A demethylase ALKBH5 is highly expressed in glioblastoma stem-like cells (GSCs). Silencing ALKBH5 suppresses the proliferation of patient-derived GSCs in vitro and in vivo. Integrated transcriptome and m6A-seq analyses revealed altered expression of select ALKBH5 target genes, including FOXM1, a critical transcription factor for the ALKBH5-dependent cell cycle gene expression. ALKBH5 binds to and demethylates FOXM1 nascent transcripts, leading to enhanced FOXM1 expression. Further, a long noncoding RNA antisense to the FOXM1 (FOXM1-AS) interacts with ALKBH5 and FOXM1 nascent transcripts and promotes their interaction. Depleting ALKBH5 and FOXM1-AS disrupted GSC tumorigenesis through the FOXM1 axis. Our work uncovers a novel function for ALKBH5 in maintaining GSC tumorigenicity and provides insight into critical roles of the m6A RNA methylation in human brain tumor.

2017-03-28 | GSE87515 | 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