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Sequencing of mRNA in AML cells upon ALKBH5 knockdown and actinomycin D treatment for different time

ABSTRACT: Sequencing of mRNA in AML cells upon ALKBH5 knockdown and actinomycin D treatment for different time

PROVIDER: PRJNA605563 | 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 in AML cells upon ALKBH5 knockdown and actinomycin D treatment for different time

Project description:To evaluate the effects of ALKBH5 KD on the mRNA stability, we conducted RNA-seq of mRNA samples enriched from AML cells with ALKBH5 knockdown and actinomycin D treatment for different time

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Sequencing of mRNA in AML cells upon ALKBH5 knockdown

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

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Sequencing of mRNA in AML cells upon ALKBH5 knockdown

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Transcriptome analyses of trophoblast upon ALKBH5 knockdown

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Actinomycin targets NPM1c-primed mitochondria in AML

Project description:Acute myeloid leukemia (AML) pathogenesis often involves a mutation in the NPM1 nucleolar chaperone, but the bases for its transforming properties and association with favorable outcome remain incompletely understood. Here we demonstrate that an oncogenic mutant form of NPM1 (NPM1c) hampers formation of PML nuclear bodies (NBs), key senescence effectors, and impairs mitochondrial function to drive an integrated stress response. Actinomycin D (ActD), an antibiotic with unambiguous clinical efficacy in relapsed/refractory NPM1c-AMLs, preferentially targets these primed mitochondria, activating cGAS signaling and boosting ROS production. The later restores PML NB formation to drive senescence of NPM1c-AMLs cells. Dual targeting of mitochondria by Venetoclax and ActD synergized for AML elimination. Our studies reveal a central role of mitochondria downstream of NPM1c and implicate a mitochondrial/ROS/PML/TP53 senescence pathway as a key effector of ActD-based, and possibly others, chemotherapies.

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Transcriptome analyses of trophoblast upon ALKBH5 knockdown

Project description:Transcriptome analyses of trophoblast upon ALKBH5 knockdown

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

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

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ALKBH5 regulates AML development and LSC as an m6A eraser

Project description:ALKBH5 regulates AML development and LSC as an m6A eraser

| PRJNA605566 | ENA