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Homo sapiens

ABSTRACT: ASH1L links histone H3 lysine 36 di-methylation to leukemia

PROVIDER: PRJNA297225 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2532560.fastq.gz	Fastqsanger.gz
	SRR2532561.fastq.gz	Fastqsanger.gz
	SRR2532562.fastq.gz	Fastqsanger.gz
	SRR2532563.fastq.gz	Fastqsanger.gz
	SRR2532564.fastq.gz	Fastqsanger.gz

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NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming

Project description:This SuperSeries is composed of the following subset Series: GSE29146: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [ChIP] GSE29147: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi] GSE29148: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO] GSE29150: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [Transduction] Refer to individual Series

2011-11-29 | E-GEOD-29305 | biostudies-arrayexpress

ASH1L links histone H3 lysine 36 di-methylation to leukemia

Project description:The histone methyltransferases MLL and ASH1L are trithorax-group proteins that interact genetically through undefined molecular mechanisms to regulate developmental and hematopoietic gene expression. Here we show that the lysine 36-dimethyl mark of histone H3 (H3K36me2) written by ASH1L is preferentially bound in vivo by LEDGF, an MLL-associated protein that co-localizes with MLL, ASH1L and H3K36me2 on chromatin genome wide. Furthermore, ASH1L facilitates recruitment of LEDGF and wild type MLL proteins to chromatin at key leukemia target genes, and is a crucial regulator of MLL-dependent transcription and leukemic transformation. Conversely KDM2A, an H3K36me2 demethylase and Polycomb-group silencing protein, antagonizes MLL-associated leukemogenesis. Our studies illuminate the molecular mechanisms underlying epigenetic interactions wherein placement, interpretation and removal of H3K36me2 contribute to the regulation of gene expression and MLL leukemia, and suggest ASH1L as a target for therapeutic intervention. Investigation of multiple transcription factors and histone modification marks in MV4-11 human leukemia cells.

2016-07-01 | E-GEOD-73528 | biostudies-arrayexpress

Genome-wide analyses of the DRB response of the histone H3 Lys36 methylation state, as well as Ash1l occupancy in mouse embryonic stem cells.

Project description:Using wild type and Ash1l ?SET mutant embryonic stem cells, against a prevalent notion, here we report di-,tri-methylation of histone H3 Lys36 occur independently of ongoing transcription. Ash1l ?SET mutant shows the impaired methylation levels in broad range of genome. Intriguingly, data implicate that a binding of retinoic acid receptor to a certain genomic region promotes installation of the tri-methylation in the retinoic acid receptor-associated gene independent of its ongoing transcription. Examination of 2 different histone modifications in 2 cell types in 2 different conditions. Examination of Ash1l occupancy in 2 different conditions.

2013-11-20 | E-GEOD-48421 | biostudies-arrayexpress

Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response

Project description:This SuperSeries is composed of the following subset Series: GSE22102: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (sequencing) GSE24774: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient DCs) GSE24776: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient MEFs) Refer to individual Series

2012-03-02 | E-GEOD-24826 | biostudies-arrayexpress

ASH1L links histone H3 lysine 36 di-methylation to leukemia

2016-07-01 | GSE73528 | GEO

Genome-wide analyses of the DRB response of the histone H3 Lys36 methylation state, as well as Ash1l occupancy in mouse embryonic stem cells.

Project description:Using wild type and Ash1l ∆SET mutant embryonic stem cells, against a prevalent notion, here we report di-,tri-methylation of histone H3 Lys36 occur independently of ongoing transcription. Ash1l ∆SET mutant shows the impaired methylation levels in broad range of genome. Intriguingly, data implicate that a binding of retinoic acid receptor to a certain genomic region promotes installation of the tri-methylation in the retinoic acid receptor-associated gene independent of its ongoing transcription.

2013-11-20 | GSE48421 | GEO

Homo sapiens

Project description:NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi]

| PRJNA142877 | ENA

Homo sapiens

Project description:NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO]

| PRJNA142879 | ENA

Homo sapiens

Project description:NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [ChIP]

| PRJNA142875 | ENA

Next Generation Sequencing of Two H3K36 methyltransferases during growth mycelia in the Magnaporthe oryzae

Project description:Di- and tri-methylation of lysine 36 on histone H3 (H3K36me2/3) are catalyzed by SET2 histone methyltransferase which play an important role in transcriptional elongation.we reveal a novel mechanism by which H3K36me2 and H3K36me3 associates with opposite transcriptional activity and Ash1 is required for the normal distribution of facultative heterochromatic modifications and stable maintenance of transcriptional silencing in eukaryotes.

2023-11-29 | GSE235261 | GEO

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