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Genome profiling of WDR5 and H3K4me3 binding in mouse embryonic stem cells

ABSTRACT: Genome profiling of WDR5 and H3K4me3 binding in mouse embryonic stem cells

PROVIDER: PRJNA739653 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14870750_1.fastq.gz	Fastqsanger.gz
	SRR14870750_2.fastq.gz	Fastqsanger.gz
	SRR14870751_1.fastq.gz	Fastqsanger.gz
	SRR14870751_2.fastq.gz	Fastqsanger.gz
	SRR14870752_1.fastq.gz	Fastqsanger.gz

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Genome profiling of WDR5 and H3K4me3 binding in mouse embryonic stem cells

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Genome profiling of WDR5, P53, H3K4Me3 binding in mouse embryonic bodies using SFEBq differetiation methods

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Essential role of lncRNA binding for WDR5 maintenance of active chromatin and embryonic stem cell pluripotency

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WDR5 high expression and its effect on tumorigenesis in leukemia

Project description:WD repeat domain 5 (WDR5) plays an important role in various biological functions through the epigenetic regulation of gene transcription. However, the oncogenic effect of WDR5 in leukemia remains largely unknown. Here, we found WDR5 expression is increased in leukemia patients. High expression of WDR5 is associated with high risk leukemia; Patients with WDR5 and MLL1 high expression have poor complete remission rate. We further identified the global genomic binding of WDR5 in leukemic cells and found the genomic co-localization of WDR5 binding with H3K4me3 enrichment. Moreover, WDR5 knockdown by shRNA suppresses cell proliferation, induces apoptosis, inhibits the expression of WDR5 targets, and blocks the H3K4me3 enrichment on the promoter of its targets. We also observed the positive correlation of WDR5 expression with these targets in the cohort study of leukemia patients. Our data reveal that WDR5 may have oncogenic effect and WDR5-mediated H3K4 methylation plays an important role in leukemogenesis.

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The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [ChIP-Seq]

Project description:WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis Using ChIP-Seq, We profiled key epigenetic marks H3K4 trimethylation in BE(2)-C neuroblastoma cells transfected with control siRNA or WDR5 siRNA-1 at N-Myc target gene promoters The results showed knockdown WDR5 significantly reduced H3K4me3 at 93.2% of N-Myc binding promoters, but only at 53.5% of N-Myc non-binding promoters. Identification of Histone H3K4 trimethylation and N-Myc binding sites in BE(2)-C cells transfected with control siRNA or WDR5 siRNA-1.

2015-12-31 | E-GEOD-70098 | biostudies-arrayexpress

ChIP-chip of siGFP- or siHOTTIP-treated foreskin fibroblasts with anti-H3K4me3, anti-H3K27me3, anti-H3K4me2, anti-histone, anti-MLL1, and anti-WDR5 antibodies on HOX tiling array

Project description:Coordinate loss of MLL1 and WDR5 occupancy caused by HOTTIP knockdown were observed in distal HOXA genes. These regions correspondingly lost H3K4me3 and H3K4me2, without changes in pan-histone or H3K27me3. human foreskin fibroblasts (CRL2091), anti-H3K4me3 (Abcam ab8580, lot#1016899), anti-H3K4me2 (Abcam ab32356, lot#947550), anti-H3K27me3 (Abcam ab4729, lot#1021724), anti-histone H3 (Abcam ab1791, lot#1025144), anti-MLL1 (gift of R. Roeder, Rockefeller University), and anti-WDR5 (gift of W. Herr, UNIL) Comparison of occupancy of MLL1 and WDR5 of siGFP and siHOTTIP foreskin fibroblasts on HOX tiling array. Human foreskin fibroblasts are transfected with siGFP or siHOTTIP for 72 hrs. The cells are harvesed and ChIP performed with H3K4me3, H4K27me3, H3K4me2, MLL1, WDR5, and histone antibodies.

2011-03-21 | E-GEOD-26540 | biostudies-arrayexpress

Wdr5 mediates self-renewal and reprogramming via the embryonic stem cell core transcriptional network

Project description:The embryonic stem (ES) cell transcriptional and epigenetic networks are critical for the maintenance of ES cell self-renewal. However, it remains unclear whether components of these networks functionally interact and if so, what factors mediate such interactions. Here we show that WD-repeat protein-5 (Wdr5), a core member of the mammalian Trithorax (trxG) complex, positively correlates with the undifferentiated state and is a novel regulator of ES cell self-renewal. We demonstrate that Wdr5, an ‘effector’ of H3K4 methylation, interacts with the pluripotency transcription factor Oct4. In concordance, genome-wide ChIP-Seq and transcriptome analyses demonstrate overlapping gene regulatory functions between Oct4 and Wdr5. We show that the Oct4-Sox2-Nanog circuitry cooperates with trxG for transcriptional activation of key self-renewal regulators. Furthermore, Wdr5 expression is required for the efficient formation of induced pluripotent stem (iPS) cells. Collectively, these findings implicate an integrated model of transcriptional and epigenetic control, mediated by select trxG members, for the maintenance of ES cell self-renewal and somatic cell reprogramming. 7 Samples

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