Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell transcriptome of ESCs upon MLL1 inhibition/deletion

ABSTRACT: Single cell transcriptome of ESCs upon MLL1 inhibition/deletion

PROVIDER: PRJNA525848 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8690190_1.fastq.gz	Fastqsanger.gz
	SRR8690190_2.fastq.gz	Fastqsanger.gz
	SRR8690188_1.fastq.gz	Fastqsanger.gz
	SRR8690188_2.fastq.gz	Fastqsanger.gz
	SRR8690189_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Transcriptome of ESCs upon MLL1 inhibition/deletion

Project description:Transcriptome of ESCs upon MLL1 inhibition/deletion

| PRJNA420025 | ENA

Transcriptome and epigenome of ESCs upon MLL1 inhibition/deletion

Project description:Transcriptome and epigenome of ESCs upon MLL1 inhibition/deletion

| PRJNA420022 | ENA

Transcriptome of ESCs upon VD3 treatment (+/-) MLL1 inhibition

Project description:Transcriptome of ESCs upon VD3 treatment (+/-) MLL1 inhibition

| PRJNA543145 | ENA

Transcriptome of ESCs upon MLL1 inhibition/deletion

Project description:This study describes the transcriptome profiling of: 1) Mll1fl/fl mESCs in LIF/Serum medium as control; 2) Mll1fl/fl mESCs with 4-OHT (Mll1-/-), MM-401 (Mll1i) in LIF/serum medium ; 2) Mll1fl/fl mESCs with 2i in LIF/serum-free (KSR) medium.

2019-12-02 | GSE107407 | GEO

Single cell transcriptome of ESCs upon MLL1 inhibition/deletion

Project description:This study describes the single-cell transcriptome profiling of: 1) Mll1fl/fl mESCs as control; 2) Mll1fl/fl mESCs with 4-OHT (Mll1-/-) or with MM-401 (Mll1i) in LIF/15KSR/5% serum KO DMEM medium on Matrigel.

2019-12-02 | GSE127943 | GEO

Occupancy of Mll1 in ESCs and transcriptome of ESCs, EpiSCs and reverted ES by MM401 (Mll1 inhibitor)

Project description:Occupancy of Mll1 in ESCs and transcriptome of ESCs, EpiSCs and reverted ES by MM401 (Mll1 inhibitor)

| PRJNA275896 | ENA

Gene expression changes upon Mll1 knockout in NUP98-HOXA9 transformed murine LSKs

Project description:We report Illumina next generation RNA sequencing (RNAseq) of NUP98-HOXA9 in vitro transformed murine LSKs upon genetic deletion of Mll1. These gene expression data illustrate that Mll1 regulates Hoxa, Hoxb and Meis1 expression in NUP98-HOXA9 transformed murine BM cells.

2016-12-11 | GSE75997 | GEO

Transcriptome and epigenome of ESCs upon MLL1 inhibition/deletion

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

2019-12-02 | GSE107408 | GEO

The histone methyltransferase activity of MLL1 is dispensable for hematopoiesis and leukemogenesis

Project description:Despite correlations between histone methyltransferase (HMT) activity and gene regulation, direct evidence that HMT activity is responsible for gene activation is sparse. We address the role of the HMT activity for MLL1, a histone H3 lysine 4 (H3K4) methyltransferase critical for maintaining hematopoietic stem cells (HSCs). Here we show that the SET domain and thus HMT activity of MLL1 is dispensable for maintaining HSCs and for supporting leukemogenesis driven by the MLL-AF9 fusion oncoprotein. Upon Mll1 deletion, histone H4 lysine 16 (H4K16) acetylation was selectively depleted at MLL1 target genes in conjunction with reduced transcription. Surprisingly, inhibition of SIRT1 was sufficient to prevent the loss of H4K16 acetylation and the reduction in MLL1 target gene expression. Thus, recruited MOF activity, and not the intrinsic HMT activity of MLL1, is central for the maintenance of HSC target genes. In addition, this work reveals a role for SIRT1 in opposing MLL1 function. 11 Samples, 5 controls and 5 KOs with antibodies H3K4me1, H3K4me3, and H3K27Ac. One input Sample.

2014-04-03 | E-GEOD-56456 | biostudies-arrayexpress

Transcriptome upon Mof deletion and Etomoxir treatment in ground-state mouse (m) ESCs

Project description:Transcriptome upon Mof deletion and Etomoxir treatment in ground-state mouse (m) ESCs

| PRJNA564621 | ENA