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ChIPseq profile of RNA polymerase (pol II), the p65 subunit of NFkB, STAT1 and STAT2 in bone marrow derived macrophages after treatment with IFNb, heat-killed Listeria monocytogenes (hkL), or both.

ABSTRACT: Using ChIP-Seq analysis we define genes induced in macrophages through synergistic transcriptional activation by NFkB and the IFNb-activated transcription factor ISGF3.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Sebastian Wienerroither

PROVIDER: E-MTAB-2972 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Response to interferons and antibacterial innate immunity in the absence of tyrosine-phosphorylated STAT1.

Majoros Andrea A Platanitis Ekaterini E Szappanos Daniel D Cheon HyeonJoo H Vogl Claus C Shukla Priyank P Stark George R GR Sexl Veronika V Schreiber Robert R Schindler Christian C Müller Mathias M Decker Thomas T

EMBO reports 20160212 3

Signal transducer and activator of transcription 1 (STAT1) plays a pivotal role in the innate immune system by directing the transcriptional response to interferons (IFNs). STAT1 is activated by Janus kinase (JAK)-mediated phosphorylation of Y701. To determine whether STAT1 contributes to cellular responses without this phosphorylation event, we generated mice with Y701 mutated to a phenylalanine (Stat1(Y701F)). We show that heterozygous mice do not exhibit a dominant-negative phenotype. Homozyg ...[more]

PMID: 26882544

Publication: 1/2

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ChIPseq profile of STAT1 binding after 2h of IFNβ treatment, in bone marrow derived macrophages isolated from WT, Stat1Y701F and Stat1-/- mice.

Project description:Using ChIP-Seq analysis we define genes induced in macrophages through transcriptional activation by STAT1 and search for the gain of function in mutant Stat1Y701F compared to the Stat1-/- mice.

2016-01-25 | E-MTAB-3597 | biostudies-arrayexpress

Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements

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Histone Demethylase Lsd1 is Required to Repress Hematopoietic Stem and Progenitor Cell Signatures During Blood Cell Maturation

Project description:Here we describe that lysine-specific demethylase 1 (Lsd1/KDM1a), which demethylates histone H3 on LysM-bM-^@M-^I4 or LysM-bM-^@M-^I9 (H3K4/K9), is an indispensible epigenetic governor of hematopoietic differentiation. Integrative genomic analysis in primary hematopoietic cells, combining global occupancy of Lsd1, genome-wide analysis of its histone substrates H3K4 mono- and di-methylation and gene expression profiling, reveals that Lsd1 represses hematopoietic stem and progenitor cell (HSPC) gene expression programs during hematopoietic differentiation. We found that Lsd1 function was not restricted to transcription start sites, but is also critical at enhancers. Loss of Lsd1 at these sites was associated with increased H3K4me1 and H3K4me2 methylation levels on HSPC genes and their derepression. Failure to fully silence HSPC genes compromised differentiation of hematopoietic stem cells and mature blood cell lineages. Our data indicate that Lsd1-mediated concurrent repression of enhancer and promoter activity of stem and progenitor cell genes is a pivotal epigenetic mechanism required for proper hematopoietic maturation. To identify direct target genes of Lsd1 in myeloid cells we mapped global occupancy of Lsd1 in 32D granuolocytic progenitor cells and compared H3K4me1/me2/me3 and H3K27ac histone modifications in Lsd1fl/fl (wild type) vs. Lsd1fl/f Mx1Cre (knockout) Gr1dim Mac1 granuolocytic progenitor cells.

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Transcriptome analysis in macrophages treated with type I interferon, heat-killed Listeria monocytogenes, or both.

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Transcription factor binding dynamics during human ES cell differentiation

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