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188 results for “NOTCH1”
Metabolic data: Inhibition of mitochondrial complex I reverses NOTCH1-driven metabolic reprogramming in T-cell acute lymphoblastic leukemia
<p>T-cell acute lymphoblastic leukemia (T-ALL) is commonly driven by activating mutations in <em>NOTCH1 </em>that facilitate glutamine oxidation. Here we identify oxidative phosphorylation (OxPhos) as a critical pathway for leukemia cell survival and demonstrate a direct relationship between <em>NOTCH1</em>, elevated OxPhos gene expression, and acquired chemoresistance in pre-leukemic and leukemic models. Disrupting OxPhos with IACS-010759, an inhibitor of mitochondrial complex I, causes potent growth inhibition through induction of metabolic shut-down and redox imbalance in <em>NOTCH1</em>-mutated and less so in <em>NOTCH1</em>-wt T-ALL cells. Mechanistically, inhibition of OxPhos induces metabolic reprogramming into glutaminolysis. We show that pharmacological blockade of OxPhos combined with inducible knock-down of glutaminase, the key glutamine enzyme, confers synthetic lethality in mice harboring <em>NOTCH1</em>-mutated T-ALL<em>. </em>We leverage this synthetic lethal interaction to demonstrate that IACS-010759 in combination with chemotherapy containing L-asparaginase, an enzyme that uncovers the glutamine dependency of leukemic cells, causes reduced glutaminolysis and profound tumor reduction in pre-clinical models of human T-ALL. In summary, this metabolic dependency of T-ALL on OxPhos provides a rational therapeutic target.</p>
Interleukin-6 (IL-6) activates the NOTCH1 signaling pathway through E-proteins in endometriotic lesions
<p><b>Context:</b> NOTCH signaling is activated in endometriotic lesions but the exact mechanisms remains unclear. Interleukin-6 (IL-6), which is increased in the peritoneal fluid of women with endometriosis, induces NOTCH1 through E-proteins including E2A and HEB in cancer development.</p> <p><b>Objective:</b> To study the role of E-proteins in inducing NOTCH1 expression under the regulation of IL-6 in endometriosis.</p> <p><b>Setting and Design:</b> The expression of E2A, HEB and NOTCH1 was first investigated in endometrium of women with endometriosis and the baboon model of endometriosis. Regulation of E-proteins and NOTCH1 expression was examined after IL-6 stimulation and siRNA mediated inhibition of E2A or/and HEB in human endometriotic epithelial cells (12Z) <i>in vitro</i>, and subsequent following <i>in vivo </i>IL-6 treatment in the mouse model of endometriosis <i>in vivo</i>.</p> <p><b>Results: </b>E2A, HEB and NOTCH1 were significantly upregulated in glandular epithelium (GE) of ectopic endometrium compared to eutopic endometrium in both women and baboon model. IL-6 treatment upregulated the expression of NOTCH1 together with E2A and HEB in 12Z cells. siRNA inhibition of E2A and HEB or HEB alone decreased NOTCH1 expression. Binding efficiency of both E2A and HEB was significantly higher at the binding sites on the human NOTCH1 promoter after IL-6 treatment. Finally, IL-6 treatment resulted in a significantly increased number of endometriotic lesions along with the increased expression of E2A, HEB and NOTCH1 in GE of the lesions compared with the vehicle treated group in an endometriosis mouse model.</p> <p><span><b>Conclusions:</b> IL-6 induced NOTCH1 expression is mediated by E-proteins in the ectopic GE cells, which may promote endometriotic lesion development. </span></p>
Single-arm Study With Bimiralisib in Patients With HNSCC Harboring NOTCH1 Loss of Function Mutations
ClinicalTrials.gov study NCT03740100. IPD Sharing: NO. Countries: 1. Publications: 1.
Interleukin-6 (IL-6) activates the NOTCH1 signaling pathway through E-proteins in endometriotic lesions
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Spns1-dependent endocardial lysosomal function drives valve morphogenesis through Notch1-signaling
<p>This doi contains raw data related to the article "Spns1-dependent endocardial lysosomal function drives valve morphogenesis through Notch1-signaling"</p> <p>Authors: Myra N. Chávez, Prateek Arora, Marco Meer, Ines J. Marques, Alexander Ernst, Rodrigo A. Morales Castro, Nadia Mercader</p> <p>the DOI of the manuscript is <a title="Persistent link using digital object identifier" href="https://doi.org/10.1016/j.isci.2024.111406" target="_blank" rel="noreferrer noopener"><span><span>https://doi.org/10.1016/j.isci.2024.111406</span></span></a></p>
Notch1 - WISP1 Axis Determines Tumor-Regulating Role of Melanoma Stromal Fibroblasts
GEO Series GSE65316. Mus musculus. 4 samples. Type: Expression profiling by array.
Telomere Length Protects Mice from Human Disease Phenotype Caused By Notch1 Haploinsufficiency
GEO Series GSE83963. Mus musculus. 15 samples. Type: Expression profiling by high throughput sequencing.
Gene expression study in SF3B1-mutated, NOTCH1-mutated and WT CLL cells
GEO Series GSE137024. Homo sapiens. 28 samples. Type: Expression profiling by array.
Gene expression profile of primary CLL cells transduced with a retrovirus expressing mutated NOTCH1
GEO Series GSE150584. Homo sapiens. 52 samples. Type: Expression profiling by high throughput sequencing.
Gene expression analysis of murine day 6 embryoid bodies (EBs ) with or without Notch1 (ICN1) induction.
GEO Series GSE19951. Mus musculus. 24 samples. Type: Expression profiling by array.
Genomic Alterations in High-risk CLL Frequently Affect Cell Cycle Key Regulators and NOTCH1‑regulated Transcription.
GEO Series GSE131114. Homo sapiens. 237 samples. Type: Genome variation profiling by SNP array.
NOTCH1 activation in breast cancer confers sensitivity to inhibition of SUMOylation
GEO Series GSE61727. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing.
Knock out of NOTCH1-bound MYC enhancer (N-Me)
GEO Series GSE57988. Mus musculus. 6 samples. Type: Expression profiling by array.
Gene expression study in WT and NOTCH1 mutated CLL cells.
GEO Series GSE75122. Homo sapiens. 10 samples. Type: Expression profiling by array.
Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate [RNA-seq]
GEO Series GSE230790. Mus musculus. 7 samples. Type: Expression profiling by high throughput sequencing.
Transcriptional profiling of human cardiomyocytes and endothelial cells derived from NOTCH1 knockout induced pluripotent stem cells (iPSCs)
GEO Series GSE195559. Homo sapiens. 30 samples. Type: Expression profiling by high throughput sequencing.
Gene expression profiling of Triple Negative Breast Cancer MB157 cells and GSI-resistant MB157R cells upon induction of Notch1 or Sox2 signaling.
GEO Series GSE262001. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Modulation of gene expression by ZNF143, THAP11 and NOTCH1 via overlapping binding sites in mammalian cells
GEO Series GSE39263. Homo sapiens; Mus musculus. 17 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
The Zmiz1-Notch1 interaction induces Myc expression to drive steady state and stress thymopoiesis [ETP and DN3]
GEO Series GSE116120. Mus musculus. 40 samples. Type: Expression profiling by high throughput sequencing.
Notch1 regulates hepatic thrombopoietin production
GEO Series GSE250529. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
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