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

PROVIDER: PRJNA771104 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16323943_1.fastq.gz	Fastqsanger.gz
	SRR16323943_2.fastq.gz	Fastqsanger.gz
	SRR16323944_1.fastq.gz	Fastqsanger.gz
	SRR16323944_2.fastq.gz	Fastqsanger.gz
	SRR16323945_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

| PRJNA771102 | ENA

ALKBH5 promotes tumor progression by decreasing RIG-I expression mediated by N6-methyladenosine-dependent HNRNPC binding in HNSCC [MeRIP-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 | GSE185885 | GEO

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

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

| PRJNA771103 | ENA

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

2022-04-13 | GSE185886 | 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

Function of HNRNPC in breast cancer cells by controlling the dsRNA-induced interferon response

Project description:Elevated expression of RNA binding protein HNRNPC has been reported in cancer cells, while the essentialness and functions of HNRNPC in tumors were not clear. We showed that repression of HNRNPC in the breast cancer cells MCF7 and T47D inhibited cell proliferation and tumor growth. Our computational inference of the key pathways and extensive experimental investigations revealed that the cascade of interferon responses mediated by RIG-I was responsible for such tumor-inhibitory effect. Interestingly, repression of HNRNPC resulted in accumulation of endogenous double-stranded RNA (dsRNA), the binding ligand of RIG-I. These up-regulated dsRNA species were highly enriched by Alu sequences and mostly originated from pre-mRNA introns that harbor the known HNRNPC binding sites. Such source of dsRNA is different than the recently well-characterized endogenous retroviruses that encode dsRNA. In summary, essentialness of HNRNPC in the breast cancer cells was attributed to its function in controlling the endogenous dsRNA and the down-stream interferon response. This is a novel extension from the previous understandings about HNRNPC in binding with introns and regulating RNA splicing.

2018-08-23 | GSE100451 | 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

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

hNRNPC iCLIP

Project description:hNRNPC iCLIP

| PRJEB2253 | ENA

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

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