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Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells

ABSTRACT: Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells

PROVIDER: PRJNA486771 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR7696230.fastq.gz	Fastqsanger.gz
	SRR7696240.fastq.gz	Fastqsanger.gz
	SRR7696250.fastq.gz	Fastqsanger.gz
	SRR7696221.fastq.gz	Fastqsanger.gz

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Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [ChIP-Seq]

Project description:Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [ChIP-Seq]

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Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [RNA-Seq]

Project description:Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [RNA-Seq]

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Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [RNA-Seq]

Project description:Identification of histone acetylation targets of Kat2a activity in murine models of acute myeloid leukaemia (AML) driven by the MLL-AF9 oncogenic fusion

2020-02-03 | GSE118768 | GEO

Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [ChIP-Seq]

Project description:Identification of histone acetylation targets of Kat2a activity in murine models of acute myeloid leukemia (AML) driven by the MLL-AF9 oncogenic fusion

2020-02-03 | GSE118576 | GEO

Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells.

Project description:Acute Myeloid Leukemia (AML) is an aggressive hematological malignancy with abnormal progenitor self-renewal and defective white blood cell differentiation. Its pathogenesis comprises subversion of transcriptional regulation, through mutation and by hijacking normal chromatin regulation. Kat2a is a histone acetyltransferase central to promoter activity, that we recently associated with stability of pluripotency networks, and identified as a genetic vulnerability in AML. Through combined chromatin profiling and single-cell transcriptomics of a conditional knockout mouse, we demonstrate that Kat2a contributes to leukemia propagation through preservation of leukemia stem-like cells. Kat2a loss impacts transcription factor binding and reduces transcriptional burst frequency in a subset of gene promoters, generating enhanced variability of transcript levels. Destabilization of target programs shifts leukemia cell fate out of self-renewal into differentiation. We propose that control of transcriptional variability is central to leukemia stem-like cell propagation, and establish a paradigm exploitable in different tumors and distinct stages of cancer evolution.

| S-EPMC7039681 | biostudies-literature

Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-02-03 | GSE118769 | GEO

Kat2a regulates hippocampal memory formation [RNA-seq]

Project description:We sequenced mRNA from 24 samples extracted from mouse CA1 tissue to generate the first CA1-specific murine transcriptome and the first CA1-transcriptome in response to environmental novelty under normal and Kat2a-loss-of-function conditions. Samples were divded in 4 groups: A: Control naM-CM-/ve (n=6), B: control novelty-exposed (n=5), C: Kat2a cKO naM-CM-/ve (n=6), D: Kat2a cKO novelty-exposed (n=7). Pairwise comparisons for AvsB, AvsC, BvsD and CvsD were performed using DESeq2.

2014-07-16 | E-GEOD-53380 | biostudies-arrayexpress

Kat2a regulates hippocampal memory formation [small RNA-seq]

Project description:We sequenced small RNAs from 12 samples extracted from mouse CA1 tissue to generate the first CA1-specific murine miRNome under normal and Kat2a-loss-of-function conditions. Samples were divded in 4 groups: A: Control (n=6), C: Kat2a cKO naÃ¯ve (n=6)

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Cochlear single-cell gene expression profiles in mice with noise-induced hidden hearing loss and noise-induced hearing loss.

Project description:Noise-induced hidden hearing loss (HHL) is a new type of hearing loss that has been identified in recent years and leads to insidious damage to the cochlea, unlike the well-known noise-induced hearing loss (NIHL). However, the cellular and molecular basis for it remains to be elucidated. Here, we established a single-cell transcriptome profile of the C57BL/6J mouse cochlea, in which we describe the transcriptome changes of individual cell types within the cochlea with HHL and NIHL. Mice in the HHL group were exposed to 110 dB of noise for 2 hours, and those in the NIHL group were exposed to 115 dB of noise for 4 hours for 3 days. The cochlea was taken 6 hours after the last noise exposure. The control group was not exposed to noise, with other conditions being the same as those in the noise-exposed group. The results of sequencing at the single-cell level help us gain a deeper understanding of the mechanisms of the development of HHL and NIHL.

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Human KAT2A/B-acetylome MudPIT

Project description:Comprehensive identification of acetylated proteins targeted by the lysine acetyltransferases KAT2A (GCN5) and KAT2B (PCAF), in human cells. KAT2A/B-dependent acetylated proteins were identified by comparing acetylated proteins in whole cell extract of control cells and cells in which KAT2A and KAT2B were simultaneously knocked down. The identification of acetylated proteins was performed using an enrichment-free approach. In order to do so, while facing the challenge of identifying low abundant acetylated peptides within a complex sample mixture, we have screened acetylated peptides starting from a large amount of material, equivalent to 50ug of protein digest (maximum loading capacity of our analytical chromatographic column). By analysing such a large amount of peptides, the level of acetylated peptides was then increased and thus acetylated peptides became easily detectable by mass spectrometry, without the need for enrichment.

2016-12-12 | PXD004669 | Pride

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