GEO DataSets

(Submitter supplied) We used microarrays to study the transcriptional networks controlled by CB-103 in HPB-ALL human cell line.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

6 Samples

Download data: CEL

(Submitter supplied) Notch pathway signaling is implicated in several human cancers. Aberrant activation and mutations of Notch signaling components are linked to tumor initiation, maintenance and resistance to cancer therapy. Several strategies, such as monoclonal antibodies (MAbs) against Notch ligands and receptors, as well as small molecule -secretase inhibitors (GSIs), have been developed to interfere with Notch receptor activation at proximal points in the pathway. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

18 Samples

Download data: TSV, TXT

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

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

12 Samples

Download data: CEL

(Submitter supplied) We used microarrays to study the transcriptional networks controlled by CB-103 in KOPT-K1 human cell line.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

6 Samples

Download data: CEL

(Submitter supplied) We discovered a new class of small molecule inhibitor that disrupts the interaction between NOTCH and RBPJ, which is the main transcriptional effector of NOTCH signaling. RBPJ Inhibitor-1 (RIN1) also blocked the functional interaction of RBPJ with SHARP, a scaffold protein that forms a transcriptional repressor complex with RBPJ in the absence of NOTCH signaling. RIN1 induced changes in gene expression resembled siRNA silencing of RBPJ rather than inhibition at the level of NOTCH itself. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

14 Samples

Download data: TXT

(Submitter supplied) The NOTCH signaling cascade, which is deregulated in T-cell acute lymphoblastic leukemia (T-ALL) and many other human cancers, offers an attractive target for molecular therapy. One approach employs gamma-secretase inhibitors (GSIs) to suppress production of the intracellular form of NOTCH (NICD), leading to cell growth arrest and apoptosis. Here we show that missense mutations or homozygous deletion of FBW7, which encodes a ubiquitin ligase that targets the NICD for destruction, mediate constitutive NICD expression. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4372

36 Samples

Download data: TXT

(Submitter supplied) NOTCH proteins regulate signaling pathways involved in cellular differentiation, proliferation and death. Overactive Notch signaling as been observed in numerous cancers and has been extensively studied in the context of T-cell acute lymphoblastic leukemia (T-ALL) where more than 50% of pateints harbour mutant NOTCH1. Small molecule modulators of these proteins would be important for understanding the role of NOTCH proteins in malignant and normal biological processes. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) NOTCH proteins regulate signaling pathways involved in cellular differentiation, proliferation and death. Overactive Notch signaling as been observed in numerous cancers and has been extensively studied in the context of T-cell acute lymphoblastic leukemia (T-ALL) where more than 50% of pateints harbour mutant NOTCH1. Small molecule modulators of these proteins would be important for understanding the role of NOTCH proteins in malignant and normal biological processes. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS3717

Platform:

GPL570

12 Samples

Download data: CEL

Analysis of HPB-ALL and KOPT-K1 cells treated with SAHM1, an antagonist of the NOTCH transcription factor. SAHM1 is an alpha-helical hydrocarbon stapled peptide derived from MAML1. Results provide insight into the specificity of the antagonistic effect of SAHM1 on gene expression driven by NOTCH.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 agent, 2 cell line sets

Platform:

GPL570

Series:

GSE18198

12 Samples

Download data: CEL

(Submitter supplied) Lipopolysaccharide (LPS)/immunue complex (IC) stimulated macrophages produce cytokine profiles that differe from LPS-stimulated inflammatory macropahges. Notch signaling is activated in LPS/IC-stimulated macrophages and inhibition of Notch signaling reduced IL-10 production. This study investigated the effect of gamma-secretase inhibitor (GSI) that suppresses Notch signaling pathway, on gene expression profiles in macrophages activated by LPS/IC.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

16 Samples

Download data: TXT

(Submitter supplied) There is evidence that brain tumor cells may hijack self-renewal mechanism that regulate stem cell maintenance during normal development. Notch signaling is fundamental for maintaining normal neural stem cells in an undifferentiated state and has been implicated in in the maintenance of brain tumor stem cells as well. We used microarrays to detail the global gene expression program in murine brain tumors lacking RBPjk, an indispensable mediator of the Notch signaling pathway in the cell nucleus.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

16 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) Genes induced by the Notch-Intracellular domain (NICD) in mouse mature T-cells (MT) are identifed. Among the induced Notch target genes we also identify those genes, which are regulated by the histone variant H2A.Z

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18480

20 Samples

Download data: TXT