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Human variation in PolII and NF-KappaB binding (ChIP-seq study with NF-KappaB)

ABSTRACT: We examined genome-wide variation in transcription factor binding in different individuals and a chimpanzee using chromatin immunoprecipitation followed by massively-parallel sequencing (ChIP-Seq). The binding sites of RNA Polymerase II (Pol II) as well as a key regulator of immune responses, NFkB, were mapped in ten HapMap lymphoblastoid cell lines derived from individuals of African, European, and Asian ancestry, including a parent-offspring trio. We also mapped gene expression in all ten human cell lines for two treatment conditions: a) no treatment and b) following induction by TNF-alpha. Genome-wide comparison of Pol II and NF-KappaB binding in ten individuals. ChIP-seq with NF-KappaB.

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Wilson

PROVIDER: E-GEOD-19485 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Variation in transcription factor binding among humans.

Kasowski Maya M Grubert Fabian F Heffelfinger Christopher C Hariharan Manoj M Asabere Akwasi A Waszak Sebastian M SM Habegger Lukas L Rozowsky Joel J Shi Minyi M Urban Alexander E AE Hong Mi-Young MY Karczewski Konrad J KJ Huber Wolfgang W Weissman Sherman M SM Gerstein Mark B MB Korbel Jan O JO Snyder Michael M

Science (New York, N.Y.) 20100318 5975

Differences in gene expression may play a major role in speciation and phenotypic diversity. We examined genome-wide differences in transcription factor (TF) binding in several humans and a single chimpanzee by using chromatin immunoprecipitation followed by sequencing. The binding sites of RNA polymerase II (PolII) and a key regulator of immune responses, nuclear factor kappaB (p65), were mapped in 10 lymphoblastoid cell lines, and 25 and 7.5% of the respective binding regions were found to dif ...[more]

PMID: 20299548

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Human variation in PolII and NF-KappaB binding (ChIP-seq study with Pol II)

Project description:We examined genome-wide variation in transcription factor binding in different individuals and a chimpanzee using chromatin immunoprecipitation followed by massively-parallel sequencing (ChIP-Seq). The binding sites of RNA Polymerase II (Pol II) as well as a key regulator of immune responses, NFkB, were mapped in ten HapMap lymphoblastoid cell lines derived from individuals of African, European, and Asian ancestry, including a parent-offspring trio. We also mapped gene expression in all ten human cell lines for two treatment conditions: a) no treatment and b) following induction by TNF-alpha. Genome-wide comparison of Pol II and NF-KappaB binding in eleven individuals. ChIP-seq study with Pol II.

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Human variation in PolII and NF-KappaB binding (ChIP-seq study with NF-KappaB)

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Human variation in PolII and NF-KappaB binding (ChIP-seq study with Pol II)

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Chromatin immunoprecipitation of human cells after lipopolysaccharide stimulation, to identify binding of NF-KappaB family members

Project description:The NF-KappaB family of transcription factors plays a critical role in numerous cellular processes, particularly the immune response. Our understanding of how the different NF-kappaB subunits act coordinately to regulate gene expression is based on a limited set of genes. We used genome-scale location analysis to identify targets of all five NF-kappaB proteins before and after stimulation of monocytic cells with bacterial lipopolysaccharide (LPS). In unstimulated cells, p50 and p52 bound to a significant number of gene promoters. p50 occupied genes together with RNA polymerase II and defined a set of genes to which other NF-kappaB proteins bound after LPS induction. In stimulated cells, genes bound by multiple NF-kappaB subunits exhibited the greatest increases in RNA polymerase II occupancy and gene expression. This study identifies novel NF-kappaB target genes, reveals how the different NF-kappaB proteins coordinate their activity and maps transcriptional regulatory networks that underlie the host response to infection.

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Human variation in PolII and NF-KappaB binding (RNA-seq study with TNF-alpha induced)

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Project description:In the central nervous system (CNS) the transcription factor NF-kappaB is a key regulator of inflammation and secondary injury processes. Following trauma or disease, the expression of NF-kappaB-dependent genes is activated, leading to both protective and detrimental effects on CNS recovery. Here we show that transgenic inactivation of astroglial NF-kappaB in mice (GFAP-IkappaBalpha-dn mice) resulted in dramatic reduction of disease severity and improvement in functional recovery following EAE. This coincided with a higher presence of leukocytes in the cord and brain of transgenic mice at the chronic phase of the disease, when the functional recovery over WT mice was the most significant. We observed that expression of proinflammatory genes in both spinal cord and cerebellum was delayed and reduced, while the loss of neuronal-specific molecules essential for synaptic transmission was limited compared to WT mice. Furthermore, death of retinal ganglion cells in affected retinas was almost abolished, suggesting the activation of neuroprotective mechanisms. Our data indicate that inhibiting NF-kappaB in astrocytes results in neuroprotective effects following EAE, directly implicating astrocytes in the pathophysiology of this disease. Keywords: time course, EAE, transgenic mice, astrocytes, inflammation, cytokines, chemokines

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