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Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression

ABSTRACT: Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression

PROVIDER: PRJNA528183 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11294608.fastq.gz	Fastqsanger.gz
	SRR11294609.fastq.gz	Fastqsanger.gz
	SRR11294610.fastq.gz	Fastqsanger.gz
	SRR11294611.fastq.gz	Fastqsanger.gz
	SRR11294612_1.fastq.gz	Fastqsanger.gz

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

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

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

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

Project description:ALKBH5 is the RNA N(6)-methyladenosine (m6A) demethylase. To understhand the function and mechnism of ALKBH5 in human acute myeloid leukemia, we compared the translational efficiency in wild-type and ALKBH5-knock-down MOLM-13 cells.

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

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

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

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

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

Project description:Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [RNA-Seq]

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

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

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

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

| PRJNA612061 | ENA