Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: N6-methyladenosine demethylase ALKBH5 promotes the development of multiple myeloma

PROVIDER: PRJNA706770 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13860400_1.fastq.gz	Fastqsanger.gz
	SRR13860400_2.fastq.gz	Fastqsanger.gz
	SRR13860401_1.fastq.gz	Fastqsanger.gz
	SRR13860401_2.fastq.gz	Fastqsanger.gz
	SRR13860398_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

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

The N6-methyadenosine (m6A) levels in PC9 cell lines.

Project description:ALKBH5 (AlkB homolog 5) has been identified as a eukaryotic demethylase, which catalyzes N6 adenosine. N6-methyladenosine (m6A) is oxidatively demethylated by ALKBH5 with α-ketoglutarate as a substrate and Fe (II) as a coenzyme. We used microarrays to detail the differential gene expression by ALKBH5 knockdown in lung cancer cell lines.

2022-06-01 | GSE165454 | GEO

Expression data from lung cancer cell lines

2022-06-01 | GSE165453 | GEO

Homo sapiens

Project description:RNA demethylase ALKBH5 promotes tumorigenesis in multiple myeloma

| PRJNA745390 | ENA

RNA demethylase ALKBH5 promotes tumorigenesis in multiple myeloma

Project description:RNA demethylase ALKBH5 promotes tumorigenesis in multiple myeloma

| PRJNA747029 | ENA

ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification

Project description:N6-methyladenosine (m6A) modification is the most prevalent RNA epigenetic regulation in eukaryotic cells. Recent studies focused on the association between m6A and non-coding RNAs. The demethylase ALKBH5 acts as critical oncogenes or tumor suppressors through multiple mechanisms in various cancers. Here, we find that ALKBH5 is highly expressed in GC tissues and is associated with poor prognosis. ALKBH5 promoted the proliferation and metastasis both in vitro and in vivo. ALKBH5 was recruited by LINC00659, which removed m6A modifications of JAK1, leading to the upregulated expression of JAK1.Since ALKBH5 and LINC00659 have oncogenic role in gastric cancer (GC) progression with poor prognosis, ALKBH5-LINC00659/m6A/JAK1 axis can be new biological mechanisms behind GC development and future therapeutic opportunities.

2024-08-17 | GSE182544 | GEO

ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [polyA]

2024-08-17 | GSE182543 | GEO

ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [2-m6A]

2024-08-17 | GSE182542 | 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

RNA demethylase ALKBH5 promotes tumorigenesis in multiple myeloma [m6A-seq]

Project description:RNA demethylase ALKBH5 promotes tumorigenesis in multiple myeloma [m6A-seq]

| PRJNA747019 | ENA