Similar studies for GEO DataSets (Select 4213) - GEO DataSets

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Items: 16

Select item 42131.

NF-kB inactivation effect on T-ALL1 cell lines

Analysis of T cell acute lymphoblastic leukemia (T-ALL) cell lines treated with a peptide that inhibits the activity of IKK, an activator of NF-kB. NF-kB pathway is downstream of oncogenic Notch1 in T-ALL. Results provide insight into the molecular basis of Notch-induced NF-kB activation in T-ALL.

Organism:: Homo sapiens

Type:: Expression profiling by array, count, 2 agent, 5 cell line sets

Platform:: GPL570
Series:: GSE20667
20 Samples

Download data: CEL

DataSet

Accession:: GDS4213

ID:: 4213

PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet

Select item 2000206672.

The Notch/Hes1 pathway sustains NF-κB activation through CYLD repression in T cell leukemia

(Submitter supplied) The NF-κB pathway is a critical regulator of the immune system and has been implicated in cellular transformation and tumorigenesis. NF-κB response is regulated by the activation state of the IκB kinase (IKK) complex and triggered by a wide spectrum of stimuli. We previously reported that NF-κB is downstream of Notch1 in T cell acute lymphoblastic leukaemia (T-ALL), however both the mechanisms involving Notch1-induced NF-κB activation and the potential importance of NF-κB in the maintenance of the disease are unknown. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Dataset:: GDS4213
Platform:: GPL570
20 Samples

Download data: CEL

Series

Accession:: GSE20667

ID:: 200020667

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000263663.

Notch/HES1-mediated PARP1 activation: A cell-type specific mechanism for tumor suppression

(Submitter supplied) Notch signaling plays both oncogenic and tumor suppressor roles, depending on cell type. In contrast to T cell acute lymphoblastic leukemia (T-ALL), where Notch activation promotes leukemogenesis, induction of Notch signaling in B-ALL leads to growth arrest and apoptosis. The Notch target Hairy/Enhancer of Split1 (HES1) is sufficient to reproduce this tumor suppressor phenotype in B-ALL, however the mechanism is not yet known. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL96
206 Samples

Download data: CEL

Series

Accession:: GSE26366

ID:: 200026366

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000278334.

Notch signaling in HSC

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

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
19 Samples

Download data: CEL

Series

Accession:: GSE27833

ID:: 200027833

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000278115.

Expression data from LSK WT, GMP WT and GMP NcstnKO

(Submitter supplied) Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2 To determine other role of Notch signaling in HSC we designed a conditional mouse model of Nicastrin deletion. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
9 Samples

Download data: CEL

Series

Accession:: GSE27811

ID:: 200027811

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000277996.

Expression data from LSK WT and LSK N1-C+

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
6 Samples

Download data: CEL

Series

Accession:: GSE27799

ID:: 200027799

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000277947.

Expression data from LSK WT and LSK NcstnKO

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
4 Samples

Download data: CEL

Series

Accession:: GSE27794

ID:: 200027794

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000063968.

Targeting the NF-κB signaling pathway in Notch1-induced T cell leukemia

(Submitter supplied) T cell acute lymphoblastic leukemia (T-ALL), unlike other ALL types, is only infrequently associated with chromosomal aberrations, but it was recently shown that the majority of TALL patients carry activating mutations in the NOTCH1 gene. However, the signaling pathways and target genes responsible for Notch1-induced neoplastic transformation remain undefined. We report here that constitutively-active Notch1 activates the NF-κB pathway transcriptionally and via the IκB kinase (IKK) complex, thereby causing increased expression of multiple well-characterized NF-κB target genes in bone marrow hematopoietic stem cells and progenitors. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL4596
3 Samples

Download data: TXT

Series

Accession:: GSE6396

ID:: 200006396

Select item 2000660149.

Global Gene Expression analysis of CUTLL1 cell lines after treatment with Perhexiline

(Submitter supplied) We identify perhexiline, a small molecule inhibitor of mitochondrial carnitine palmitoyltransferase-1, as a HES1-signature antagonist drug with robust antileukemic activity against NOTCH1 induced leukemias in vitro and in vivo.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL11154
6 Samples

Download data: CSV

Series

Accession:: GSE66014

ID:: 200066014

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20006587210.

Expression data from CUTLL1 cells infected with shHES1

(Submitter supplied) To formally address the biological activity of HES1 in vitro, we measured the transcriptional effect of HES1 inactivation infectiing CUTLL1 leukemia cell lines with shHES1 HES1 knockdown triggered apoptosis in human T-ALL lymphoblasts. We show that HES1 inactivation induces programmed cell death in leukemia lymphoblasts

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL10558
4 Samples

Download data: TXT

Series

Accession:: GSE65872

ID:: 200065872

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20006586311.

Expression data from Hes1 conditional knock-out NOTCH1-induced leukemias

(Submitter supplied) To formally address the biological activity of Hes1 in vivo, we tested the interaction between oncogenic NOTCH1 and acute Hes1 loss in a retroviral-transduction bone marrow transplantation model of NOTCH-induced T-ALL Forced expression of activated NOTCH1 in this model typically results in full leukemia transformation 5-10 weeks later.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL6887
6 Samples

Download data: TXT

Series

Accession:: GSE65863

ID:: 200065863

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20005692112.

Expression analysis of common myeloid progenitors (CMPs) expressing Hes1

(Submitter supplied) High levels of Hes1 expression are frequently found in BCR-ABL-positive chronic myelogenous leukemia in blast crisis (CML-BC). In mouse bone marrow transplantation (BMT) models, co-expression of BCR-ABL and Hes1 induces CML-BC–like disease; however the underlying mechanism remained elusive. Here, based on gene expression analysis, we show that MMP-9 is upregulated by Hes1 in common myeloid progenitors (CMPs). more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
2 Samples

Download data: CEL

Series

Accession:: GSE56921

ID:: 200056921

Select item 20004746613.

Notch-HES1 signaling axis controls hemato-endothelial fate decisions of human embyronic and induced pluripotent cells

(Submitter supplied) Notch signaling regulates several cellular processes including cell fate decisions and proliferation in both invertebrates and mice. However, comparatively less is known about the role of Notch during early human development. Here, we examined the function of Notch signaling during hematopoietic lineage specification from human pluripotent stem cells (hPSCs) of both embryonic and adult fibroblast origin. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL96
8 Samples

Download data: CEL

Series

Accession:: GSE47466

ID:: 200047466

Select item 20013061414.

HES1 and HES4 have both unique and overlapping roles as downstream mediators of Notch-dependent hematopoietic lineage decisions in human

(Submitter supplied) In both mouse and human, Notch1 activation is the main initial driver to induce T-cell development in hematopoietic progenitor cells. The initiation of this developmental process coincides with Notch1-dependent repression of differentiation towards other hematopoietic lineages. Although well described in mice, the role of the individual Notch1 target genes during these hematopoietic developmental choices is still unclear in human. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18573
18 Samples

Download data: TXT

Series

Accession:: GSE130614

ID:: 200130614

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20001013615.

Gene expression profile upon forced Notch1 activation in LS174T cells

(Submitter supplied) The cell line was modified to express activated form of Notch1 (NICD1 of mouse origin) upon Doxycycline addition to the culture medium. Generation was performed by using the T-rex system (invitrogen), following manufacturer's instruction. Keywords: Genetic modification

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL1293
4 Samples

Download data: GPR

Series

Accession:: GSE10136

ID:: 200010136

Select item 20003826416.

In vivo disruption of Rb-E2F-Ezh2 signaling loop causes bladder cancer development

(Submitter supplied) Bladder cancer (BC) is a highly prevalent human disease in which Rb pathway inactivation and epigenetic alterations are common events. However, the connection between these two processes is still poorly understood. Here we show that the in vivo inactivation of all Rb family genes in the mouse urothelium is sufficient to initiate BC development. The characterization of the mouse tumors revealed multiple molecular features of human BC, including the activation of E2F transcription factor and subsequent Ezh2 expression, and the activation of several signaling pathways previously identified as highly relevant in urothelial tumors. more...