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Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of primary human acute myeloid leukemia (AML) cells

ABSTRACT: Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of primary human acute myeloid leukemia (AML) cells

PROVIDER: PRJNA464346 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7126420.fastq.gz	Fastqsanger.gz
	SRR7126421.fastq.gz	Fastqsanger.gz
	SRR7126422.fastq.gz	Fastqsanger.gz
	SRR7126423.fastq.gz	Fastqsanger.gz
	SRR7126424.fastq.gz	Fastqsanger.gz

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Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of primary human acute myeloid leukemia (AML) cells

Project description:To explore the function of Mitochondrial Fission 1 (FIS1) in acute myeloid leukemia (AML), we used shRNA to knock down the expression of FIS1 in primary human AML cells and performed RNA-seq experiments to profile global gene expression changes upon FIS1 depletion.

2018-06-01 | GSE114109 | GEO

Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of leukemia cell line MOLM-13 cells

Project description:To explore the function of Mitochondrial Fission 1 (FIS1) in acute myeloid leukemia (AML), we used shRNA to knock down the expression of FIS1 in leukemia cell line MOLM-13 cells and performed RNA-seq experiments to profile transcriptional changes upon FIS1 depletion.

2018-06-01 | GSE114111 | GEO

Mitochondrial Fission 1 (FIS1) knockdown effect on the H3K27Ac status of leukemia cell line MOLM-13 cells

Project description:To examine if loss of FIS1 would alter the H3K27Ac status of leukemic cells, we used shRNA to knock down the expression of FIS1 in leukemic cell line MOLM-13 cells and performed H3K27Ac CHIP-seq to characterize any changes in the H3K27Ac marks upon loss of FIS1.

2018-06-01 | GSE114106 | GEO

Role of mitochondrial fission-related genes in mitochondrial morphology and energy metabolism in mouse embryonic stem cells

Project description:Here we aimed to investigate the function of mitochondrial fission genes in embryonic stem cells (ESCs). Homozygous knockout ESC lines, namely, Fis1-/- , Mff-/- , and Dnm1l-/- ESCs, were generated using the CRISPR-Cas9 system. After then, we analyzed whole genome expression profile for characterizing cellular responses by incomplete mitochondrial fission.

2020-04-21 | GSE148959 | GEO

Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of leukemia cell line MOLM-13 cells

Project description:Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of leukemia cell line MOLM-13 cells

| PRJNA464347 | ENA

Mitochondrial Fission 1 (FIS1) knockdown effect on the H3K27Ac status of leukemia cell line MOLM-13 cells

Project description:Mitochondrial Fission 1 (FIS1) knockdown effect on the H3K27Ac status of leukemia cell line MOLM-13 cells

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Genome-wide synthetic lethal CRISPR screen identifies FIS1 as a genetic interactor of ALS-linked C9ORF72

Project description:Mutations in the C9ORF72 gene are the most common cause of amyotrophic lateral sclerosis (ALS). Both toxic gain of function and loss of function pathogenic mechanisms have been proposed. Accruing evidence from mouse knockout studies point to a role for C9ORF72 as a regulator of immune function. To provide further insight into its cellular function, we performed a genome-wide synthetic lethal CRISPR screen in human myeloid cells lacking C9ORF72. We discovered a strong synthetic lethal genetic interaction between C9ORF72 and FIS1, which encodes a mitochondrial membrane protein involved in mitochondrial fission and mitophagy. Mass spectrometry experiments revealed that in C9ORF72 knockout cells, FIS1 strongly bound to a class of immune regulators that activate the receptor for advanced glycation end (RAGE) products and trigger inflammatory cascades. These findings present a novel genetic interactor for C9ORF72 and suggest a compensatory role for FIS1 in suppressing inflammatory signaling in the absence of C9ORF72.

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Sharp2019 - AML

Project description:The paper describes a model of acute myeloid leukaemia. Created by COPASI 4.26 (Build 213) This model is described in the article: Optimal control of acute myeloid leukaemia Jesse A. Sharp, Alexander P Browning, Tarunendu Mapder, Kevin Burrage, Matthew J Simpson Journal of Theoretical Biology 470 (2019) 30–42 Abstract: Acute myeloid leukaemia (AML) is a blood cancer affecting haematopoietic stem cells. AML is routinely treated with chemotherapy, and so it is of great interest to develop optimal chemotherapy treatment strategies. In this work, we incorporate an immune response into a stem cell model of AML, since we find that previous models lacking an immune response are inappropriate for deriving optimal control strategies. Using optimal control theory, we produce continuous controls and bang-bang controls, corre- sponding to a range of objectives and parameter choices. Through example calculations, we provide a practical approach to applying optimal control using Pontryagin’s Maximum Principle. In particular, we describe and explore factors that have a profound influence on numerical convergence. We find that the convergence behaviour is sensitive to the method of control updating, the nature of the control, and to the relative weighting of terms in the objective function. All codes we use to implement optimal control are made available. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

2024-09-02 | BIOMD0000000798 | BioModels

Acute Myeloid Leukemia (AML) patient xenografts

Project description:Acute Myeloid Leukemia (AML) patient xenografts

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Epigenetic dysregulation of the Drp1 binding partners MiD49 and MiD51 increases mitotic mitochondrial fission and promotes pulmonary arterial hypertension: mechanism and therapeutic implications

Project description:Mitotic fission is increased in hyperproliferative, apoptosis-resistant diseases, such as pulmonary arterial hypertension (PAH). PAH’s fissogenic phenotype includes activation of the fission mediator, dynamin related protein 1 (Drp1), which must complex with its adaptor proteins to cause fission. Drp1-induced fission has been therapeutically targeted in experimental PAH. Here we examine the role of two recently discovered, poorly understood, Drp1 adapter proteins, mitochondrial dynamics protein of 49 and 51 kDa (MiD49 and MiD51) in normal vascular cells and explore the role of their dysregulation in the pathogenesis of PAH. MiDs are increased in PAH PASMC. This accelerates Drp1-mediated mitotic fission, which increases cell proliferation and decreases apoptosis. Silencing MiDs (but not Fis1 or MFF) promotes mitochondrial fusion and G1-phase cell cycle arrest through an ERK1/2 and CDK4-dependent mechanism. Augmenting MiDs in normal cells causes fission and recapitulates the PAH phenotype. MiD upregulation results from decreased microRNA-34a-3p (miR-34a-3p) expression. Circulatory miR34a-3p expression is decreased in PAH patients as well as in preclinical models of PAH. Silencing MiDs or augmenting miR-34a-3p regresses experimental PAH. We used microarrays to identify differences in miR expression in pulmonary artery smooth muscle cells (PASMC) taken from either pulmonary arterial hypertension patients or healthy controls

2018-01-31 | GSE108707 | GEO

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