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ALKBH5 regulates AML development and LSC as an m6A eraser

ABSTRACT: ALKBH5 regulates AML development and LSC as an m6A eraser

PROVIDER: PRJNA605566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11048300.fastq.gz	Fastqsanger.gz
	SRR11048301.fastq.gz	Fastqsanger.gz
	SRR11048302.fastq.gz	Fastqsanger.gz
	SRR11048303.fastq.gz	Fastqsanger.gz
	SRR11048304.fastq.gz	Fastqsanger.gz

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Sequencing of mRNA with N6-methyladenosine (m6A) modification in AML cells upon ALKBH5 knockdown or overexpression

Project description:To identify the potential mRNA targets of ALKBH5, we conducted m6A-seq with mRNA samples enriched from AML cells with ALKBH5 knockdown or overexpression

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ALKBH5 K235 acetylation regulates the RNA m6A profiles

Project description:We performed the transcripome-wild m6A-sequencing to compare the m6A profiles of negative control (NC) HeLa cells and ALKBH5 KO HeLa cells stably re-expressing wild type ALKBH5 (WT) or its mutant K235R (K235R)

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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

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ALKBH5 regulates AML development and LSC as an m6A eraser

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

2020-05-26 | GSE144984 | GEO

Post-translational Modification of RNA m6A Demethylase ALKBH5 Regulates ROS-induced DNA Damage Response

Project description:Faithful genome integrity maintenance plays an essential role in cell survival. Here, we identify the RNA demethylase ALKBH5 as a key regulator that protects cells from DNA damage and apoptosis during reactive oxygen species (ROS)-induced stress. We find that ROS significantly induces global mRNA N6-methyladenosine (m6A) levels by modulating ALKBH5 post-translational modifications (PTMs), leading to the rapid and efficient induction of thousands of genes involved in a variety of biological processes including DNA damage repair. Mechanistically, ROS promotes ALKBH5 SUMOylation through activating ERK/JNK signaling, leading to inhibition of ALKBH5 m6A demethylase activity by blocking substrate accessibility. Moreover, ERK/JNK/ALKBH5-PTMs/m6A axis is activated by ROS in hematopoietic stem/progenitor cells (HSPCs) in vivo in mice, suggesting a physiological role of this molecular pathway in the maintenance of genome stability in HSPCs. Together, our study uncovers a molecular mechanism involving ALKBH5 PTMs and increased mRNA m6A levels that protect genomic integrity of cells in response to ROS.

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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.

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

Project description:We here report ALKBH5, a m6A RNA demethylase, as a crucial oncogene in multiple myeloma (MM). Using various MM models, we demonstrated a critical requirement of ALKBH5 for MM cell proliferation in vitro and in vivo. To identify the potential mRNA targets of ALKBH5, we conducted m6A-seq with mRNA samples enriched from MM cells with or without ALKBH5 knockdown.

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m6A methylation regulates hypoxia-induced pancreatic cancer glycolytic metabolism through ALKBH5-HDAC4-HIF1α positive feedback loop

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