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Comparative gene expression analysis in OCI-LY19 isogenic cell lines with SETD1B mutation or KMT2D+SETD1B double mutants.

ABSTRACT: Comparative gene expression analysis in OCI-LY19 isogenic cell lines with SETD1B mutation or KMT2D+SETD1B double mutants.

PROVIDER: PRJNA1140257 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29999158_1.fastq.gz	Fastqsanger.gz
	SRR29999158_2.fastq.gz	Fastqsanger.gz
	SRR29999159_1.fastq.gz	Fastqsanger.gz
	SRR29999159_2.fastq.gz	Fastqsanger.gz
	SRR29999160_1.fastq.gz	Fastqsanger.gz

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Comparative gene expression analysis in OCI-LY19 isogenic cell lines with SETD1B mutation or KMT2D+SETD1B double mutants.

Project description:The translocation t(14;18) activates BCL2 and is considered the initiating genetic lesion in most follicular lymphomas (FL). Surprisingly, FL patients fail to respond to the BCL2 inhibitor, Venetoclax. We show that mutations and deletions affecting the histone lysine methyltransferase SETD1B (KMT2G) occur in 7% of FLs and in 16% of diffuse large B cell lymphomas (DLBCL). Deficiency in SETD1B confers striking resistance to Venetoclaxand to an experimental MCL-1 inhibitor. SETD1B also acts as a tumor suppressor andcooperates with loss ofKMT2Din lymphoma development in vivo. Consistently, loss of SETD1B in human lymphomas typically coincides with loss of KMT2D. Mechanistically, SETD1B is required for the expression of several pro-apoptotic BCL2 family proteins. Conversely, inhibitors of the KDM5 histoneH3K4demethylases restore BIM and BIK expression and synergize with Venetoclax inSETD1B-deficient lymphomas.

2024-08-23 | GSE273152 | GEO

Comparative gene expression analysis in OCI-LY8 isogenic cell lines with SETD1B mutation or WT control.

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H3K5me3 modifications in OCI-LY19 cells with and without SETD1B mutations.

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Comparative gene expression analysis in OCI-LY8 isogenic cell lines with SETD1B mutation or WT control.

Project description:Comparative gene expression analysis in OCI-LY8 isogenic cell lines with SETD1B mutation or WT control.

| PRJNA1140256 | ENA

H3K5me3 modifications in OCI-LY19 cells with and without SETD1B mutations.

Project description:H3K5me3 modifications in OCI-LY19 cells with and without SETD1B mutations.

| PRJNA1140255 | ENA

MLL4 (KMT2D) inactivating mutations lead to focal loss of H3K4me1/2 and deregulated gene expression in B cell lymphomas

Project description:We identified KMT2D target loci in OCI-LY7 by ChIPseq. KMT2D ChIPseq was carried out in the LY7 cell line (n=1).

2015-08-28 | E-GEOD-67314 | biostudies-arrayexpress

MLL4 (KMT2D) inactivating mutations lead to focal loss of H3K4me1/2 and deregulated gene expression in B cell lymphomas

Project description:We identified KMT2D target loci in OCI-LY7 by ChIPseq.

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Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

Project description:Histone 3 lysine 4 trimethylation (H3K4me3) is an epigenetic mark found at active gene promoters and CpG islands. H3K4me3 is essential for mammalian development, yet mechanisms underlying its genomic targeting are poorly understood. H3K4me3 methyltransferases SETD1B and MLL2 are essential for oogenesis. We investigated changes in H3K4me3 in Setd1b conditional knockout (cKO) GV oocytes using ultra-low input ChIP-seq, in complement to DNA methylation and gene expression analysis. Setd1b cKO oocytes showed a redistribution of H3K4me3, with a marked loss at active gene promoters associated with downregulated gene expression. Remarkably, many regions gained H3K4me3 in Setd1b cKOs, in particular those that were DNA hypomethylated, transcriptionally inactive and CpG-rich. All of these are hallmarks of MLL2 targets; thus, loss of SETD1B appears to enable enhanced MLL2 activity. Our work reveals two distinct, complementary mechanisms of genomic targeting of H3K4me3 in oogenesis, with SETD1B linked to transcriptional activity and MLL2 to CpG content.

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Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

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Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

2022-01-17 | GSE167984 | GEO