Similar Datasets
Project description:Genome-wide maps of HHEX binding
| PRJNA615887 | ENA
Project description:By performing chromatin immunoprecipitation coupled with ultra-high-throughput sequencing (ChIP-seq), we find that RAP1 binds to telomeres as well as to extra-telomeric sites through the (TTAGGG)2 consensus motif. Extra-telomeric RAP1 binding sites are particularly abundant at subtelomeric regions, and this is in agreement with preferential deregulation of subtelomeric genes in Rap1-deficient cells. Significantly, more than 70% of extratelomeric RAP1 binding sites are located in the vicinity of known genes and about 40% of the genes deregulated in Rap1-null cells contain binding sites for RAP1, suggesting a role of RAP1 in transcriptional control. Examination of RAP1 binding by CHIP-seq in two independent wild-type mefs using as negative control two independent RAP1-deleted mefs
2010-07-10 | E-GEOD-20867 | biostudies-arrayexpress
Project description:By performing chromatin immunoprecipitation coupled with ultra-high-throughput sequencing (ChIP-seq), we find that RAP1 binds to telomeres as well as to extra-telomeric sites through the (TTAGGG)2 consensus motif. Extra-telomeric RAP1 binding sites are particularly abundant at subtelomeric regions, and this is in agreement with preferential deregulation of subtelomeric genes in Rap1-deficient cells. Significantly, more than 70% of extratelomeric RAP1 binding sites are located in the vicinity of known genes and about 40% of the genes deregulated in Rap1-null cells contain binding sites for RAP1, suggesting a role of RAP1 in transcriptional control.
2010-07-10 | GSE20867 | GEO
Project description:To identify WT and RNA-binding-domain-mutated (RBDmut) ERα binding sites on DNA, we performed ChIP-seq of FLAG-tagged ERα.
2021-08-01 | GSE173629 | GEO
Project description:We report the high-throughput profiling of ISL1-binding sites in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide ISL1-binding maps of SGC7901 cells. This study provides a prediction of regulated genes by the ISL1.
2019-03-06 | GSE122056 | GEO
Project description:We report the high-throughput profiling of ISL1-binding sites in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide ISL1-binding maps of Huh7 cells. This study provides a prediction of regulated genes by the ISL1.
2019-02-01 | GSE77957 | GEO
Project description:We report the high-throughput profiling of PBX3-binding sites under liver cancer stem cell reprogramming driven by PBX3 overexpression. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide PBX3-binding maps of SMMC-7721 cells. This study provides a prediction of regulated genes by the PBX3.
2015-09-24 | GSE71260 | GEO
Project description:The pancreas and liver arise from a common pool of progenitors in the foregut endoderm; however, the underlying molecular mechanisms driving this lineage diversification are not fully understood. We combined human pluripotent stem cell guided differentiation and sequential CRISPR-Cas9 loss-of-function screening to uncover regulators of pancreatic specification. Here we report the discovery of a cell-intrinsic requirement for HHEX, a transcription factor (TF) associated with diabetes susceptibility. HHEX promotes pancreatic differentiation through cooperation with pancreatic TFs as well as common TFs like FOXA2 that are shared by both pancreas and liver differentiation programs. Furthermore, HHEX restricts differentiation plasticity, and deletion of HHEX shifts FOXA2 interaction towards cooperation with HNF4A, driving liver differentiation. Therefore, HHEX safeguards pancreatic differentiation by promoting lineage specification while simultaneously restricting cell fate plasticity, demonstrating how organ domain demarcation requires fine tuning of TF cooperation.
2022-04-29 | GSE181478 | GEO
Project description:Estrogen receptor beta (ERbeta) has potent anti-proliferative and anti-inflammatory properties, suggesting that ER beta-selective agonists might be a new class of therapeutic and chemopreventative agents. To understand how ER beta regulates genes, we identified genes regulated by the unliganded and liganded forms of ER alpha and ER beta in U2OS cells. Microarray data demonstrated that virtually no gene regulation occurred with unliganded ER alpha, whereas many genes were regulated by estradiol (E2). These results demonstrate ER alpha requires a ligand to regulate a single class of genes. In contrast, ER beta regulated three classes of genes. Class I genes were regulated primarily by unliganded ER beta. Class II genes were regulated only with E2, whereas Class III genes were regulated by both unliganded ER beta and E2. There were 453 Class I genes, 258 Class II genes and 83 Class III genes. To explore the mechanism whereby ER beta regulates different classes of genes ChIP-seq was performed to identify ER beta binding sites and adjacent transcription factor motifs in regulated genes. AP1 binding sites were more enriched in Class I genes, whereas ERE, NFKB1 and SP1 sites were more enriched in class II genes. ER beta bound to all three classes of genes demonstrating that ER beta binding is not responsible for differential regulation of genes by unliganded and liganded ER beta. The coactivator, NCOA2 was differentially recruited to several target genes. Our findings indicate that the unliganded and liganded forms of ER beta regulate three classes of genes by interacting with different transcription factors and coactivators. Examination of ER beta binding sites in U2OS cells with or without E2 treatment
2010-05-12 | E-GEOD-21770 | biostudies-arrayexpress
Project description:The Hematopoietically-expressed homeobox (Hhex) transcription factor is overexpressed in human myeloid leukemias. Conditional knockout models of murine acute myeloid leukemia (AML) indicate that Hhex maintains leukemia stem cell self-renewal by enabling Polycomb-mediated epigenetic repression of the Cdkn2a tumor suppressor locus, encoding p16Ink4a and p19Arf. However, whether Hhex overexpression also affects hematopoietic differentiation is unknown. To study this, we retrovirally overexpressed Hhex in hematopoietic progenitors. This enabled serial replating of myeloid progenitors, leading to the rapid establishment of IL-3-dependent promyelocytic cell lines. Use of a Hhex-ERT2 fusion protein demonstrated that continuous nuclear Hhex is required for transformation, and structure function analysis demonstrated a requirement of the DNA binding and N-terminal repressive domains of Hhex for promyelocytic transformation. This included the N-terminal Pml interaction domain, although deletion of Pml failed to prevent Hhex-induced promyelocyte transformation, implying other critical partners. Furthermore, deletion of p16Ink4a or p19Arf did not promote promyelocyte transformation, indicating that repression of distinct Hhex target genes is required for this process. Indeed, transcriptome analysis showed that Hhex overexpression resulted in repression of several myeloid developmental genes. To test potential for Hhex overexpression to contribute to leukemic transformation, Hhex-transformed promyelocyte lines were rendered growth factor-independent using a constitutively active IL-3 receptor common b subunit (bcV449E). The resultant cell lines resulted in a rapid promyelocytic leukemia in vivo. Thus Hhex overexpression can contribute to myeloid leukemia via multiple mechanisms including differentiation blockade and enabling epigenetic repression of the Cdkn2a locus.
2018-01-30 | GSE109793 | GEO