Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA115505 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To study the correlation between sequence motif appearance, transcription factor binding and aberrant hypermethylation in the cell lines, we performed ChIP-on-chip analyses (on CpG island microarrays) for the transcription factors Sp1, NRF1 and YY1 in normal peripheral blood monocytes. Keywords: ChIP-on-Chip; comparative genomic hybridization Transcription factor bound genomic DNA was enriched using ChIP. On each microarray, the enriched material was compared to the genomic input to identify transcription factor bound regions. Two biological replicates were analysed for each factor.
2010-06-05 | E-GEOD-16078 | biostudies-arrayexpress
Project description:To study the correlation between sequence motif appearance, transcription factor binding and aberrant hypermethylation in the cell lines, we performed ChIP-on-chip analyses (on CpG island microarrays) for the transcription factors Sp1, NRF1 and YY1 in normal peripheral blood monocytes. Keywords: ChIP-on-Chip; comparative genomic hybridization
2010-03-31 | GSE16078 | GEO
Project description:ChIP-chip analyses of five transcription factors (ERR1, GABP, NRF1, CREB and YY1) PRC coactivator and RNA polymerase II in XTC.UC1 cells compared to non specific IP (IgG or input) seven factors studied: ERR1, GABP, NRF1, CREB, YY1, PRC, RNAPolII
2017-11-07 | GSE106597 | GEO
Project description:Transcriptome analysis of peripheral blood monocytes
| PRJNA350561 | ENA
Project description:Mammalian development is regulated by the interplay of tissue-specific and ubiquitously expressed transcription factors, such as Sp1. Sp1 knock-out mice die in utero with multiple phenotypic aberrations, but the underlying molecular mechanism of this differentiation failure has been elusive. Here we used conditional knock-out mice as well as the differentiation of mouse ES cells as a model to address this issue. To this end we examined differentiation potential, global gene expression patterns and Sp1 target regions in Sp1 wild-type and deficient cells representing different stages of hematopoiesis. Sp1-/- cells progress through most embryonic stages of blood cell development but cannot complete terminal differentiation. For most Sp1 target and non-target genes, gene expression is unaffected by Sp1 inactivation. However, Cdx and multiple Hox genes are stage-specific targets of Sp1 and are down-regulated at an early stage. As a consequence, expression of genes involved in hematopoietic specification are progressively deregulated, highlighting the regulatory hierarchy of hematopoietic specification. Our work demonstrates that the early absence of active Sp1 sets a cascade in motion that culminates in a failure of terminal hematopoietic differentiation and emphasizes the role of ubiquitously expressed transcription factors for tissue-specific gene regulation. Two ChIP-Seq data from Sp1 transcription factor obtained from FLK+ and progenitor cells
2014-06-12 | E-GEOD-52496 | biostudies-arrayexpress
Project description:The ability to chronicle transcription factor binding events throughout the development of an organism would facilitate mapping of transcriptional networks that control cell fate decisions. We describe a method for permanently recording protein-DNA interactions in mammalian cells. We endow transcription factors with the ability to deposit a transposon into the genome near to where they bind. The transposon becomes a M-bM-^@M-^\Calling CardM-bM-^@M-^] the transcription factor leaves behind to record its visit to the genome. The locations of the Calling Cards can be determined by massively-parallel DNA sequencing. We show that the transcription factor SP1 fused to the piggyBac transposase directs insertion of the piggyBac transposon near SP1 binding sites. The locations of transposon insertions are highly reproducible, and agree with sites of SP1-binding determined by ChIP-seq. Genes bound by SP1 are more likely to be expressed in the HCT116 cell line we used, and SP1-bound CpG islands show a strong preference to be unmethylated. This method has the potential to trace transcription factor binding throughout cellular and organismal development in a way that has heretofore not been possible. These data contain mapped insertion sites from the piggyBac (PB) transposon into HCT116 cell line and sequenced using an Illumina GAII analyzer. The first set contains the insertion sites of transposons mapped from the wild-type PB transposase and the second set contains the insertion sites of transposons mapped with the PB transposase fused to the transcription factor SP1. Other sequencing data present are ChIP-seq data for SP1 in the HCT116 cell line and RNA-seq data.
2011-12-31 | E-GEOD-34791 | biostudies-arrayexpress
Project description:The ability to chronicle transcription factor binding events throughout the development of an organism would facilitate mapping of transcriptional networks that control cell fate decisions. We describe a method for permanently recording protein-DNA interactions in mammalian cells. We endow transcription factors with the ability to deposit a transposon into the genome near to where they bind. The transposon becomes a “Calling Card” the transcription factor leaves behind to record its visit to the genome. The locations of the Calling Cards can be determined by massively-parallel DNA sequencing. We show that the transcription factor SP1 fused to the piggyBac transposase directs insertion of the piggyBac transposon near SP1 binding sites. The locations of transposon insertions are highly reproducible, and agree with sites of SP1-binding determined by ChIP-seq. Genes bound by SP1 are more likely to be expressed in the HCT116 cell line we used, and SP1-bound CpG islands show a strong preference to be unmethylated. This method has the potential to trace transcription factor binding throughout cellular and organismal development in a way that has heretofore not been possible.
2011-12-31 | GSE34791 | GEO
Project description:Yin and yang 1 (YY1) is a well-known zinc-finger transcription factor with crucial roles in normal development and malignancy. YY1 acts both as a repressor and an activator of gene expression. We have identified 23 individuals with de novo mutations or deletions of YY1 and phenotypic features that define a syndrome of cognitive impairment, behavioral alterations, intrauterine growth retardation, feeding problems, and various congenital malformations. Our combined clinical and molecular data define the ‘YY1 syndrome’ as a haploinsufficiency syndrome. Through immunoprecipitation of YY1-bound chromatin from person-derived cells, using antibodies recognizing both ends of the protein, we show that YY1 deletions and missense mutations lead to a global loss of YY1 binding, with a preferential retention at high-occupancy sites. Finally, we uncover a widespread loss of H3K27 acetylation in particular on the YY1-bound enhancers, underscoring a crucial role for YY1 in enhancer regulation. Collectively, these results define a clinical syndrome caused by haploinsufficiency of YY1 through dysregulation of key transcriptional regulators.
2017-05-19 | GSE98477 | GEO
Project description:Yin and yang 1 (YY1) is a well-known zinc-finger transcription factor with crucial roles in normal development and malignancy. YY1 acts both as a repressor and an activator of gene expression. We have identified 23 individuals with de novo mutations or deletions of YY1 and phenotypic features that define a syndrome of cognitive impairment, behavioral alterations, intrauterine growth retardation, feeding problems, and various congenital malformations. Our combined clinical and molecular data define the ‘YY1 syndrome’ as a haploinsufficiency syndrome. Through immunoprecipitation of YY1-bound chromatin from person-derived cells, using antibodies recognizing both ends of the protein, we show that YY1 deletions and missense mutations lead to a global loss of YY1 binding, with a preferential retention at high-occupancy sites. Finally, we uncover a widespread loss of H3K27 acetylation in particular on the YY1-bound enhancers, underscoring a crucial role for YY1 in enhancer regulation. Collectively, these results define a clinical syndrome caused by haploinsufficiency of YY1 through dysregulation of key transcriptional regulators.
2017-05-19 | GSE98476 | GEO
Project description:DNA Methylome in Human Peripheral Blood Monocytes
| PRJNA171224 | ENA