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Inhibition of Lysine-Specific Demethylase-1 in Myelodysplastic Syndrome Progenitors Restores Differentiation of CD141Hi Conventional Dendritic Cells

ABSTRACT: Inhibition of Lysine-Specific Demethylase-1 in Myelodysplastic Syndrome Progenitors Restores Differentiation of CD141Hi Conventional Dendritic Cells

PROVIDER: PRJNA544952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9130210.fastq.gz	Fastqsanger.gz
	SRR9130220.fastq.gz	Fastqsanger.gz
	SRR9130230.fastq.gz	Fastqsanger.gz
	SRR9130211.fastq.gz	Fastqsanger.gz
	SRR9130221.fastq.gz	Fastqsanger.gz

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Inhibition of Lysine-Specific Demethylase-1 in Myelodysplastic Syndrome Progenitors Restores Differentiation of CD141Hi Conventional Dendritic Cells

Project description:Immunotherapeutic approaches to treat patients with myelodysplastic syndromes (MDS) show promise but progress is hindered by our incomplete knowledge of the immunologic milieu. In a recent phase I trial, we found that vaccination of MDS patients against the tumor antigen NY-ESO-1 activated antigen-specific adaptive immune responses in patients with higher numbers of CD141Hi conventional dendritic cells (cDCs). In solid tumor models, the CD141Hi cDC is critical for initiating anti-tumor immune responses but its impact in myeloid malignancies is unknown. In a series of studies using human samples and mouse models, we tested the hypothesis that MDS patients would exhibit decreased quantity and quality of CD141Hi cDCs due to myeloid dysplasia. Overall, we found CD141Hi cDCs were decreased in MDS patients’ bone marrow and that decreased numbers of CD141Hi cDCs were associated with reduced overall survival. MDS patients had reduced numbers of DC committed progenitors and their progenitors expressed lower levels of the transcription factor interferon regulatory factor-8 (IRF8), a master regulator of CD141Hi cDC differentiation. Induction of IRF8 expression in mouse, healthy human and MDS patient progenitors using an inhibitor of lysine-specific demethylase-1 (LSD1) increased CD141Hi cDC differentiation. These data reveal a previously unrecognized factor of the immune microenvironment in MDS and suggest intriguing connections between epigenetic regulation of CD141Hi cDC differentiation in MDS and the ability to translate these mechanisms to improve immunotherapy for MDS patients.

2019-11-23 | GSE131792 | GEO

CpG islands recruit a histone H3 lysine 36 demethylase

Project description:This SuperSeries is composed of the following subset Series: GSE18588: CpG islands recruit a histone H3 lysine 36 demethylase [Illumina sequencing data] GSE21201: CpG islands recruit a histone H3 lysine 36 demethylase [Agilent data] Refer to individual Series

2010-04-26 | E-GEOD-21202 | biostudies-arrayexpress

Inhibition of lysine-specific demethylase 1 inhibition in glioblastoma

Project description:Inhibition of lysine-specific demethylase 1 inhibition in glioblastoma

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Uncoupling Histone Modification Crosstalk by Engineering Lysine Demethylase LSD1

Project description:Uncoupling Histone Modification Crosstalk by Engineering Lysine Demethylase LSD1

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Lysine-specific demethylase 1 target genes in brown adipocytes

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Targeting Lysine Demethylase 5 (KDM5) in Mantle Cell Lymphoma

Project description:Targeting Lysine Demethylase 5 (KDM5) in Mantle Cell Lymphoma

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CpG islands recruit a histone H3 lysine 36 demethylase [Illumina sequencing data]

Project description:Eukaryotic gene expression profiles are largely defined by transcription factors that recognize specific DNA sequences in gene regulatory regions and impact RNA polymerase recruitment and transcription. In addition to specific core promoter regulatory elements, up to 70% of genes in higher eukaryotes are also characterized by an overrepresentation of cytosine/guanine base pairs (CpGs) surrounding promoters and gene regulatory units. These features, called CpG islands, were identified over twenty years ago but there remains little mechanistic evidence to suggest how these enigmatic elements contribute to promoter function, with the exception that they are refractory to epigenetic silencing by DNA methylation. Here we uncover a role for CpG islands in buffering gene regulatory elements from repressive histone H3 lysine 36 methylation by directly recruiting the H3K36 specific lysine demethylase enzyme KDM2A. KDM2A is recruited to CpG islands by a zinc finger CxxC (ZF-CxxC) domain that specifically recognizes CpG DNA and is blocked by DNA methylation. This capacity to sense the epigenetic methylation state of DNA constrains KDM2A to non-methylated CpG islands. Importantly, these observations suggest CpG islands may function to delineate gene regulatory elements from bulk chromatin by recruiting factors that create unique chromatin architecture. This study provides information about binding of lysine demethylase enzyme KDM2A in mouse embryonic stem cells.

2010-04-27 | E-GEOD-18588 | biostudies-arrayexpress

Lysine-specific demethylase 1 metastasis of androgen-independent PCa cells

Project description:Lysine-specific demethylase 1 metastasis of androgen-independent PCa cells

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The Lysine Demethylase KDM7A Regulates Immediate Early Genes in Neurons.

Project description:The Lysine Demethylase KDM7A Regulates Immediate Early Genes in Neurons.

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Uncoupling Histone Modification Crosstalk by Engineering Lysine Demethylase LSD1

Project description:Biochemical crosstalk between two or more histone modifications is often observed in epigenetic enzyme regulation but its functional significance in cells has been difficult to discern. Prior enzymatic studies have revealed that Lys14 acetylation of histone H3 can inhibit Lys4 demethylation by lysine specific demethylase 1 (LSD1). Here we have engineered a mutant form of LSD1, Y391K, which renders the nucleosome demethylase activity of LSD1 insensitive to Lys14 acetylation. Y391K LSD1 knockin cells show increased repression of a set of genes associated with cellular adhesion. Chromatin profiling revealed that the cis-regulatory regions of these silenced genes display a higher level of H3 Lys14 acetylation than the baseline in unedited, parental cells. Y391K LSD1 knockin cells show diminished H3 mono-methyl Lys4 in the vicinity of these silenced genes, consistent with a role for enhanced LSD1 demethylase activity in these regions. These findings illuminate the functional consequences of disconnecting histone modification crosstalk for a key epigenetic enzyme in gene and chromatin regulation.

2024-05-08 | GSE243231 | GEO

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