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

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

PROVIDER: PRJNA1140256 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29999485_1.fastq.gz	Fastqsanger.gz
	SRR29999485_2.fastq.gz	Fastqsanger.gz
	SRR29999486_1.fastq.gz	Fastqsanger.gz
	SRR29999486_2.fastq.gz	Fastqsanger.gz
	SRR29999487_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:Comparative gene expression analysis in OCI-LY19 isogenic cell lines with SETD1B mutation or KMT2D+SETD1B double mutants.

| PRJNA1140257 | ENA

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.

2024-08-23 | GSE273153 | GEO

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

2024-08-23 | GSE273154 | GEO

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

Expression data of H838 KRAS mutation isogenic cell lines

Project description:To explore the distinct mechanism of KRAS G12V and G12D mutation. We used microarray to explore the distinct differences in gene expression profiles of H838 KRAS mutation isogenic cell lines

2020-05-21 | GSE119146 | GEO

Expression data of H838 KRAS mutation isogenic cell lines

Project description:Expression data of H838 KRAS mutation isogenic cell lines

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H3K4me2 profiling in OCI-Ly1 and OCI-Ly7 cell lines.

Project description:Define and compare H3K4me2 enrichment in OCI-Ly1 and OCI-Ly7 cell lines.

2015-08-28 | GSE67381 | GEO

H3K4me2 profiling in OCI-Ly1 and OCI-Ly7 cell lines.

Project description:Define and compare H3K4me2 enrichment in OCI-Ly1 and OCI-Ly7 cell lines. Using ChIP-seq, we examined the H3K4me2 genomic enrichment locations in two biological replicates in each cell line

2015-08-28 | E-GEOD-67381 | biostudies-arrayexpress

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.

2022-01-17 | GSE167986 | GEO

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