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Effect of knockout of ALKBH5 on gene expression and m6A modifications during IRI in mice

ABSTRACT: Effect of knockout of ALKBH5 on gene expression and m6A modifications during IRI in mice

PROVIDER: PRJNA930466 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23308035_1.fastq.gz	Fastqsanger.gz
	SRR23308035_2.fastq.gz	Fastqsanger.gz
	SRR23308036_1.fastq.gz	Fastqsanger.gz
	SRR23308036_2.fastq.gz	Fastqsanger.gz
	SRR23308037_1.fastq.gz	Fastqsanger.gz

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Effect of knockout of ALKBH5 on gene expression and m6A modifications during IRI in mice

Project description:To identify the direct m6A demethylation targets of ALKBH5 at the onset of renal IRI, we performed methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) using RNA isolated from IRI mouse kidney of WT and KO mice 24h after I/R (WT n=3 vs. KO n=3)

2023-02-05 | GSE224289 | GEO

m6a modifications following morphine exposure or Alkbh5 siRNA in primary cortical neuron cultures

Project description:m6a modified RNA and unmodified RNA were quantified in primary neuronal cultures following either siRNA knockdown of Alkbh5 or chronic morphine exposure for 3 days. The goal was to identify mRNA that have m6A modifications following one or more treatment conditions.

2024-09-01 | GSE243685 | GEO

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

m6A Demethylase ALKBH5 attenuates doxorubicin-induced cardiotoxicity via posttranscriptional stabilization of Rasal3

Project description:The clinical application of anthracyclines such as doxorubicin (DOX) is limited due to their cardiotoxicity. N6-methyladenosine (m6A) plays an essential role in numerous biological processes. However, the roles of m6A and m6A demethylase ALKBH5 in DOX-induced cardiotoxicity (DIC) remain unclear. In this research, DIC models were constructed using Alkbh5-knockout (KO), Alkbh5-knockin (KI), and Alkbh5-myocardial-specific knockout (ALKBH5flox/flox, αMyHC-Cre) mice. Cardiac function and DOX-mediated signal transduction were investigated. As a result, both Alkbh5 whole-body KO and myocardial-specific KO mice had increased mortality, decreased cardiac function, and aggravated DIC injury with severe myocardial mitochondrial damage. Conversely, ALKBH5 overexpression alleviated DOX-mediated mitochondrial injury, increased survival, and improved myocardial function. Mechanistically, ALKBH5 regulated the expression of Rasal3 in an m6A-dependent manner through posttranscriptional mRNA regulation and reduced Rasal3 mRNA stability, thus activating RAS3, inhibiting apoptosis through the RAS/RAF/ERK signaling pathway, and alleviating DIC injury. These findings indicate the potential therapeutic effect of ALKBH5 on DIC.

2023-03-08 | GSE224215 | GEO

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

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 | GSE182542 | GEO

Genome-wide maps of m6a state in RA FLSs with or without ALKBH5 knockdown.

Project description:To investigate how ALKBH5 modulates RA FLSs functions, we conducted m6A sequencing (MeRIP-seq) of RA FLSs. Consistent with previous studies, in both scramble controls and ALKBH5 knockdown cells, m6A modifications were highly enriched within the GGAC motif. m6A peaks are located mainly in the protein-coding region (CDS) and 3’ untranslated region (3’ UTR) of mRNA transcripts

2023-12-31 | GSE203269 | GEO

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

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

Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [m6A-seq]

Project description:ALKBH5 is the RNA N(6)-methyladenosine (m6A) demethylase. To under sthand the function and mechnism of ALKBH5 in human acute myeloid leukemia, we compared the m6A profiling in wild-type, ALKBH5-knock-down, and ALKBH5 rescue THP1 cells.

2020-05-27 | GSE128520 | GEO

Transcriptome-wide m6A Methylation Profiling of Wild Type and ALKBH5-/- Peritoneal Macrophages by m6A-seq

Project description:By performing m6A-seq analysis on the peritoneal macrophages that derived from ALKBH5-/- mice and littermate mice infected with or without vesicular stomatitis virus (VSV), we want to investigate whether ALKBH5 deficiency-mediated m6A RNA methylation contributes to the regulation of its target genes expression. m6A-seq analysis revealed enriched and specific m6A peaks on the transcript of ALKBH5-targeted gene, which were substantially increased in ALKBH5-deficient peritoneal macrophages than that in wild-type cells whatever infected with or without VSV. Meanwhile we didn’t observe up-regulation of m6A signal on VSV in ALKBH5-deficient cells; and also didn't find significant difference of m6A signals on IFN-β mRNA between ALKBH5-deficient and wild type cells whatever infected with or without VSV. These demonstrated that deficiency of ALKBH5 controls viral replication by increasing the m6A modification of ALKBH5 target gene to regulate its expression.

2019-08-22 | GSE127732 | GEO

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