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ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [MeRIP-seq]

ABSTRACT: To determine the targets underlying ALKBH5 during head and neck squamouse cell carcinoma progression, Methylated RNA immunoprecipitation (MeRIP) with an m6A specific antibody followed by RNA sequencing (MeRIP-seq) and next generation sequencing were combined to screen the potential targets haboring m6A modificatios and mRNA level alteration after ALKBH5 knockdown in a HNSCC cell line.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185885 | GEO | 2022/04/13

REPOSITORIES: GEO

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ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [RNA-seq]

Project description:To determine the targets underlying ALKBH5 during head and neck squamouse cell carcinoma progression, Methylated RNA immunoprecipitation (MeRIP) with an m6A specific antibody followed by RNA sequencing (MeRIP-seq) and next generation sequencing were combined to screen the potential targets haboring m6A modificatios and mRNA level alteration after ALKBH5 knockdown in a HNSCC cell line.

2022-04-13 | GSE185886 | GEO

Identification of ALKBH5 targets in osteosarcoma by methyl RNA immunoprecipitation [MeRIP-seq]

Project description:To identify potential target mRNAs that are demethylated by ALKBH5, meRIP-seq with a m6A antibody was conducted in 143B osteosarcoma cells transfected with scrambled or ALKBH5-siRNA.

2022-06-28 | GSE154529 | 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

ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [MeRIP-seq]

Project description:ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [MeRIP-seq]

| PRJNA771104 | ENA

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 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [meRIP-seq]

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 | GSE248526 | GEO

ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-04-13 | GSE185888 | GEO

The interacted proteins of ALKBH5 and FTO identified by IP-mass

Project description:Since m6A demethylases (FTO and ALKBH5) have been reported to be involved in pre-mRNA splicing regulation, we hypothesized that dynamic m6A distribution during mRNA maturation might involve removal of m6A in internal exons by FTO or ALKBH5 accompanied by splicing factors. To explore this we performed pull-down assays coupled with protein mass spectrometry.

2022-12-09 | PXD038705 | Pride

The effects of ALKBH5 on m6A mRNA modification in the liver [MeRIP-seq]

Project description:Through m6A mRNA-profiling, we aim to characterize the m6A mRNA changes in the liver between Alkbh5flox/flox and Alkbh5-HKO mice.

2025-02-27 | GSE227175 | GEO

m6A meRIP-Seq from Ythdf2CTL pre-leukemic cells

Project description:The mRNA m6A reader YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To understand the role of YTHDF2 in AML, we generated m6A meRIP-seq libraries form Ythdf2fl/fl (Ythdf2CTL) pre-leukemic cells.

2019-04-05 | E-MTAB-6791 | biostudies-arrayexpress

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