GEO DataSets

Analysis of Notch1-dependent TLL cell line CUTLL1 treated with γ-secretase-inhibitor (GSI) to block Notch signaling, subjected to GSI washout to induce Notch1 reactivation, and incubated up to 4hr with translational inhibitor cycloheximide. Results provide insight into Notch1 function in TLL.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 3 agent, 3 cell line, 7 protocol sets

Platform:

GPL570

Series:

GSE29544

45 Samples

Download data: CEL

(Submitter supplied) Notch1 regulates gene expression by associating with the DNA-binding factor RBPJ and is oncogenic in murine and human T cell progenitors. Using ChIP-Seq, we find that in human and murine T-LL genomes Notch1 binds preferentially to promoters, to RBPJ binding sites, and near imputed ZNF143, Ets and Runx sites. ChIP-Seq confirmed that ZNF143 binds to ~40% of Notch1 sites. Notch1/ZNF143 sites are characterized by high Notch1 and ZNF143 signals, frequent co-binding of RBPJ (generally through sites embedded within ZNF143 motifs), strong promoter bias, and relatively low mean levels of activating chromatin marks. more...

Organism:

Homo sapiens; Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL9052 GPL9185

16 Samples

Download data: BED

(Submitter supplied) Notch is normally activated by cleavage and nuclear translocation of its intracellular domain (ICN1), which turns on downstream target genes. Human T cell acute lymphoblastic leukemia (T-ALL), an aggressive immature T cell malignancy, is associated with Notch 1 gain-of-function mutations in more than 50% of the cases. Efforts to date to identify direct Notch1 targets have been confounded by the lack of a method to turn Notch1 on in a controlled fashion in T-ALL cells that are poised to respond to Notch signals. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4289

Platform:

GPL570

45 Samples

Download data: CEL

(Submitter supplied) The main oncogenic driver in T-lymphoblastic leukemia (T-LL) is NOTCH1, which activates genes by forming chromatin-associated Notch transcription complexes. Gamma-secretase (GSI) inhibitor treatment prevents NOTCH1 nuclear localization, but most genes with NOTCH1 binding sites are insensitive to GSI. Here, we demonstrate that fewer than 10% of NOTCH1 binding sites show dynamic changes in NOTCH1 occupancy when T-LL cells are toggled between the Notch-on and –off states with GSI. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

15 Samples

Download data: BED

(Submitter supplied) Epstein-Barr Virus Nuclear Antigen 2 (EBNA2) gene regulation through the cell RBPJ transcription factor (TF) is essential for conversion of resting B-lymphocytes (RBLs) into Lymphoblastoid Cell Lines (LCLs). ChIP-seq investigation of EBNA2 and RBPJ sites in LCL DNA found EBNA2 at 5151 and RBPJ at 10,529 sites. EBNA2 was 72% localized with RBPJ, predominantly at intergenic and intronic sites and only 14% at promoter sites. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9052

6 Samples

Download data: BED

(Submitter supplied) Notch is needed for T cell development and is a common oncogenic driver in T cell acute lymphoblastic leukemia. Myc is a critical target of Notch in normal and malignant pre-T cells, but how Notch regulates Myc is unknown. Here, we identify a distal enhancer located >1 Mb 3' of human and murine Myc that binds Notch transcription complexes and physically interacts with the Myc proximal promoter. The Notch1 binding element in this region activates reporter genes in a Notch-dependent, cell context-specific fashion that requires a conserved Notch complex binding site. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9185

9 Samples

Download data: BED

(Submitter supplied) In this study we investigated the genome wide DNA binding profile of ZNF143 and ICN1 in human and murine cells. We also analyzed the expression profile in human cells after overexpression or knockdown of ZNF143.

Organism:

Mus musculus; Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL10999 GPL11154 GPL11002

17 Samples

Download data: TXT, WIG

(Submitter supplied) From the cell-based investigation, RBPJ is one of the few proteins retained on chromatin during cell division. ChIP-seq experiments were performed to understand the binding pattern of RBPJ between interphase and mitosis and to identify the genes requiring RBPJ binding for the maintenance of transcriptional memory. Our results indicate that ~60% of RBPJ occupancy in interphase is retained on mitotic chromatin, and that accounts for 80% of RBPJ in mitosis. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: BED

(Submitter supplied) We report the application of ChIP Seq to study the Epstein Barr Virus Nuclear Antigen EBNA3A, EBNA3B, EBNA3C, an essential transcriptional regulator involved in the transformation of Resting B Lymphocytes to the immortalized Lymphoblast Cell Lines.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

3 Samples

Download data: WIG

(Submitter supplied) Notch signalling plays crucial roles in mediating cell fate choices in all metazoans largely by specifying the transcriptional output of one cell in response to a neighbouring cell. The DNA-binding protein RBPJ is the principle effector of this pathway in mammals and together with the transcription factor moiety of Notch (NICD) it regulates the expression of target genes. The prevalent view presumes that RBPJ statically occupies consensus binding sites while exchanging repressors for activators in response to NICD. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:

GPL11002 GPL13112

33 Samples

Download data: BED, RPKM, WIG

(Submitter supplied) Vascular endothelial cells upregulate the Notch ligand Jagged1 in response to inflammatory activation. Here we show that abrogation of endothelial Notch1 signaling impairs induction of key inflammatory target genes. Accordingly, inducible endothelial-targeted knockout of the canonical Notch transcription factor RBPJ reduces inflammation in a murine model of contact hypersensitivity, while overexpression of constitutive active Notch1 has the opposite effect. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL18573 GPL20301

15 Samples

Download data: BED, BW

(Submitter supplied) Notch1 is a key regulator of endothelial cell behaviour. This experiment was designed to identify genes regulated by Notch1 signaling in inflammatory activated mouse endothelial cells.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL17400

20 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

4 related Platforms

59 Samples

Download data: BED, BW, CEL, IDAT

(Submitter supplied) Inflammatory activation of endothelial cells enables leukocyte recruitment to tissues. We here investigate how Notch1 signaling affects the transcriptional profile of inflammatory activated human umbilical vein cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

12 Samples

Download data: IDAT

(Submitter supplied) Proinflammatory activation of endothelial cells leads to recruitment of leukocytes by upregulation of adhesion molecules and presentation of chemoattractants. In response to such activation there is also a strong shift in the endothelial expression of Notch ligands, with downregulation of Dll4 and a upregulation of JAG1. To assess whether Jagged1 would affect the endothelial activation profile, we suppressed JAG1 expression during IL-1β-induced activation by means of siRNA and performed a genome-wide transcriptome analysis. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

12 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL21103 GPL17021

60 Samples

Download data

(Submitter supplied) Notch1 signaling ramps up to very high levels in order to drive CD4-CD8- double-negative (DN) thymocytes to the CD4+CD8+ double-positive (DP) stage. During this important phase of T-cell development, which is known as the DN-DP transition, it is unclear whether the Notch1 complex simply strengthens its signal output as an isolated unit or recruits cofactors to amplify its signals. We previously showed that the PIAS-like coactivator Zmiz1 is a direct and context-dependent cofactor of Notch1 in T-cell leukemia. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

40 Samples

Download data: TXT

(Submitter supplied) Notch1 signaling ramps up to very high levels in order to drive CD4-CD8- double-negative (DN) thymocytes to the CD4+CD8+ double-positive (DP) stage. During this important phase of T-cell development, which is known as the DN-DP transition, it is unclear whether the Notch1 complex simply strengthens its signal output as an isolated unit or recruits cofactors to amplify its signals. We previously showed that the PIAS-like coactivator Zmiz1 is a direct and context-dependent cofactor of Notch1 in T-cell leukemia. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

20 Samples

Download data: XLSX

(Submitter supplied) Epstein-Barr-Virus (EBV) Nuclear Antigens EBNALP and EBNA2 are co-expressed in EBV infected B-lymphocytes and are critical for Lymphoblastoid Cell Line (LCL) growth. EBNALP removes NCOR1 and RBPJ repressive complexes from promoter and enhancer sites and EBNA2 mostly activates transcription from distal enhancers. ChIP-seqs found EBNALP at 19,224 LCL sites, which were 33% promoter associated. EBNALP was associated with 10 transcription factor (TF) clusters that included YY1(63%), SP1(62%), PAX5(59%), BATF(50%), IRF4(49%), RBPJ(43%), ETS1(39%), PU.1(37%), RAD21(33%), NF-kB(31%), TBLR1(26%), ZNF143(24%), CTCF(23%), SMC3(21%), and EBF(17%). more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

2 Samples

Download data: TXT

(Submitter supplied) Murine ES cells were grown on confluent OP-9 and differentiated along the hematopoitic lineage. To assess the effects of Notch in hematopoiesis, activated Notch was overexpressed from Day 5 to Day 8.

Organism:

Human alphaherpesvirus 2; Mus musculus cytomegalovirus 2; Homo sapiens; Mus musculus; Human alphaherpesvirus 1; Human betaherpesvirus 5; Human immunodeficiency virus 1; Merkel cell polyomavirus; Rattus norvegicus; human gammaherpesvirus 4; JC polyomavirus; Human gammaherpesvirus 8; Betapolyomavirus macacae; Murid gammaherpesvirus 4; Betapolyomavirus hominis

Type:

Non-coding RNA profiling by array

Platform:

GPL11432

9 Samples

Download data: GPR