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Mitochondrial carrier homolog 2 (MTCH2) is necessary for AML survival

ABSTRACT: Mitochondrial carrier homolog 2 (MTCH2) is necessary for AML survival

PROVIDER: PRJNA615031 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11412300_1.fastq.gz	Fastqsanger.gz
	SRR11412300_2.fastq.gz	Fastqsanger.gz
	SRR11412301_1.fastq.gz	Fastqsanger.gz
	SRR11412301_2.fastq.gz	Fastqsanger.gz
	SRR11412302_1.fastq.gz	Fastqsanger.gz

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Mitochondrial carrier homolog 2 (MTCH2) is necessary for AML survival

Project description:Through a CRISPR screen to identify mitochondrial genes necessary for the growth of AML cells, we identified the mitochondrial outer membrane protein MTCH2 (Mitochondrial Carrier Homolog 2). In AML, knockdown of MTCH2 decreased growth, reduced engraftment potential of stem cells and induced differentiation. Inhibiting MTCH2 altered in AML cells increased nuclear pyruvate and pyruvate dehydrogenase that induced histone acetylation and subsequently promoted the differentiation of AML cells. Thus, we have defined a new mechanism by which mitochondria and metabolism regulate AML stem cells and gene expression.

2020-03-25 | GSE147508 | GEO

Mitochondrial carrier homolog 2 (MTCH2) regulates the differentiation of AML cells by controlling pyruvate entry into the mitochondria, nuclear localization of pyruvate dehydrogenase complex and H3 and H4 histone acetylation

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Carrier Subclass

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Mimp/Mtch2-GFP overexpression in transgenic mice kidney

Project description:Metabolic dysfunctions, such as fatty liver, obesity and insulin resistance, are among the most common contemporary diseases worldwide. Mimp/Mtch2 is a mitochondrial carrier protein homologue that leads to mitochondrial depolarization, localizes to the mitochondria and induces accumulation of fat vesicles. Transgenic mice overexpressing Mimp/Mtch2 develop fatty livers and kidneys and exhibit high blood glucose levels. The mechanism of lipid accumulation in the kidney has not been fully determined. In this study we performed a differential gene expression profile of fatty compared to non-fatty kidneys of Mimp/Mtch2-GFP transgenic mice, fed on high fat diet. RNA samples for microarray gene expression profiling were obtained from four Mimp/Mtch2-GFP mice, two samples of low fat kidneys and two of fatty kidneys.

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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.

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Project description:Chemoresistance is the leading cause of acute myeloid leukemia (AML)-related deaths, and elucidation of the mechanisms of AML chemoresistance is necessary to effectively target this process. Here, we performed genome wide CRISPR-Cas9 screening to identify key molecules regulating AML chemoresistance.

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IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells

Project description:IPO11 regulates the nuclear import of BZW1/2 and is necessary for AML cells and stem cells

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