Relevant bibliographies by topics / Notch1 Receptor

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Academic literature on the topic 'Notch1 Receptor'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Notch1 Receptor"

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Wu, Guangyu, Svetlana Lyapina, Indranil Das, Jinhe Li, Mark Gurney, Adele Pauley, Inca Chui, Raymond J. Deshaies, and Jan Kitajewski. "SEL-10 Is an Inhibitor of Notch Signaling That Targets Notch for Ubiquitin-Mediated Protein Degradation." Molecular and Cellular Biology 21, no. 21 (November 1, 2001): 7403–15. http://dx.doi.org/10.1128/mcb.21.21.7403-7415.2001.

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ABSTRACT Notch receptors and their ligands play important roles in both normal animal development and pathogenesis. We show here that the F-box/WD40 repeat protein SEL-10 negatively regulates Notch receptor activity by targeting the intracellular domain of Notch receptors for ubiquitin-mediated protein degradation. Blocking of endogenous SEL-10 activity was done by expression of a dominant-negative form containing only the WD40 repeats. In the case of Notch1, this block leads to an increase in Notch signaling stimulated by either an activated form of the Notch1 receptor or Jagged1-induced signaling through Notch1. Expression of dominant-negative SEL-10 leads to stabilization of the intracellular domain of Notch1. The Notch4 intracellular domain bound to SEL-10, but its activity was not increased as a result of dominant-negative SEL-10 expression. SEL-10 bound Notch4 via the WD40 repeats and bound preferentially to a phosphorylated form of Notch4 in cells. We mapped the region of Notch4 essential for SEL-10 binding to the C-terminal region downstream of the ankyrin repeats. When this C-terminal fragment of Notch4 was expressed in cells, it was highly labile but could be stabilized by the expression of dominant-negative SEL-10. Ubiquitination of Notch1 and Notch4 intracellular domains in vitro was dependent on SEL-10. Although SEL-10 interacts with the intracellular domains of both Notch1 and Notch4, these proteins respond differently to interference with SEL-10 function. Thus, SEL-10 functions to promote the ubiquitination of Notch proteins; however, the fates of these proteins may differ.
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Takam Kamga, Paul, Federica Resci, Giada Dal Collo, Annalisa Adamo, Riccardo Bazzoni, Angela Mercuri, Massimiliano Bonifacio, and Mauro Krampera. "Prognostic Impact of Notch Signaling in Acute Myeloid Leukemia (AML)." Blood 132, Supplement 1 (November 29, 2018): 5242. http://dx.doi.org/10.1182/blood-2018-99-118701.

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Abstract Background: Notch signaling is a developmental pathway involved in normal and malignant hematopoiesis. Mutations in Notch genes lead to T-ALL and are associated with poor prognosis in B-CLL. However its role in AML is still under investigation, with controversial results. In addition, although the pathway consists of 4 receptors and 5 ligands, many studies are mostly based on single receptor or ligand. Aims: This study was conducted to determine if the expression level of each Notch receptor and ligand are associated with known prognostic factors and patient's survival. Methods: AML primary cells were collected from 79 AML patients after informed consent. The follow-up was for 36 months. Flow cytometry analysis was used to study the expression of each Notch receptor and ligand. Prognostics or risk factors considered were sex, white blood counts, FAB and cytogenetics. The Mann-Whitney test was used for analyzing differences in expression levels between two groups. Spearman test was used for correlation between Notch expression levels and prognostics factors. Differences in overall (OS) and progression free (PFS) survival were established through Gehan-Breslow-Wilcoxon test. Results: Consistently with previous findings, we found expression of Notch1, Notch2, Notch3, Notch4, Jagged1, Jagged2 and DLL3 in AML samples. There were no differences in expression levels between male and female. For each receptor or ligand, higher expression levels were found in more immature samples (M0, M1, and M2). Notch3, Notch4 and Jagged2 were enriched in adverse cytogenenetics risk groups compared to favorable cytogenetics risk patients. Then, for each receptor or ligand, patients were divided into two groups; patients with higher expression levels and patients with lower expression levels. Analyzing OS and PFS, we found that patients with lower expression levels of Notch4, Jagged2 and DLL3 displayed a longer survival compared to patients with higher expression levels. Conclusion: Given its oncogenic role in T-ALL and other malignancies Notch1 has been the more studied receptors in hematological malignancies. However, we have previously demonstrated that Notch4, DLL3 and Jagged2 are all involved in survival of AML and B-ALL cells. Studying the prognostic value of all Notch receptors and ligands, the current research clearly shows that higher levels of Notch4 and Jagged2 are found in poor cytogenetics risk groups and are associated with a shorter patient's survival. These demonstrations suggest that expression levels of Notch receptors and ligands in AML patient's samples at diagnostic could stand as prognostic marker for clinical care. Disclosures No relevant conflicts of interest to declare.
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Liu, Xiaoxia, Qingqing Luo, Yanfang Zheng, Xiaoping Liu, Ying Hu, Weifang Liu, Minglian Luo, Yin Zhao, and Li Zou. "NOTCH4 signaling controls EFNB2-induced endothelial progenitor cell dysfunction in preeclampsia." Reproduction 152, no. 1 (July 2016): 47–55. http://dx.doi.org/10.1530/rep-16-0132.

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Preeclampsia is a serious complication of pregnancy and is closely related to endothelial dysfunction, which can be repaired by endothelial progenitor cells (EPCs). The DLL4/NOTCH–EFNB2 (ephrinB2) cascade may be involved in the pathogenesis of preeclampsia by inhibiting the biological activity of EPCs. In addition, both NOTCH1 and NOTCH4, which are specific receptors for DLL4/NOTCH, play critical roles in the various steps of angiogenesis. However, it has not been determined which receptor (NOTCH1, NOTCH4, or both) is specific for the DLL4/NOTCH–EFNB2 cascade. Accordingly, we performed a series of investigations to evaluate it. EFNB2 expression was examined when NOTCH4 or NOTCH1 was downregulated, with or without DLL4 treatment. Then, the effects of NOTCH4 on EPC function were detected. Additionally, we analyzed NOTCH4 and EFNB2 expression in the EPCs from preeclampsia and normal pregnancies. Results showed that NOTCH4 downregulation led to decreased expression of EFNB2, which maintained the same level in the presence of DLL4/NOTCH activation. By contrast, NOTCH1 silencing resulted in a moderate increase in EFNB2 expression, which further increased in the presence of DLL4/NOTCH activation. The downregulation of NOTCH4 resulted in an increase of EPC biological activity, which was similar to EFNB2 silencing. NOTCH4 expression, consistent with the EFNB2 level, increased notably in preeclampsia EPCs compared with the controls. These findings suggest that NOTCH4, not NOTCH1, is the specific receptor for the DLL4/NOTCH–EFNB2 cascade. Blockade of this cascade may enhance the angiogenic property of EPCs, and act as a potential target to promote angiogenesis in patients with preeclampsia.
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Tu, Jian, Yang Li, Zhiqiang Hu, and Zhongbin Chen. "Radiosurgery inhibition of the Notch signaling pathway in a rat model of arteriovenous malformations." Journal of Neurosurgery 120, no. 6 (June 2014): 1385–96. http://dx.doi.org/10.3171/2013.12.jns131595.

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Object Notch signaling has been suggested to promote the development and maintenance of arteriovenous malformations (AVMs), but whether radiosurgery inhibits Notch signaling pathways in AVMs is unknown. The aim of this study was to examine molecular changes of Notch signaling pathways following radiosurgery and to explore mechanisms of radiosurgical obliteration of “nidus” vessels in a rat model of AVMs. Methods One hundred eleven rats received common carotid artery–to–external jugular vein anastomosis to form an arteriovenous fistula (AVF) model. Six weeks postoperatively, dilated small vessels and capillaries formed a nidus. The rats with AVFs received 25-Gy radiosurgery. The expression of Notch1 and Notch4 receptors and their ligands, Delta-like1 and Delta-like4, Jagged1, Notch downstream gene target HES1, and an apoptotic marker caspase-3 in nidus vessels in the AVF rats was examined immunohistochemically and was quantified using LAS-AF software at 7 time points over a period of 42 days postradiosurgery. The interaction events between Notch1 receptor and Jagged1, as well as Notch4 receptor and Jagged1, were quantified in nidus vessels in the AVF rats using proximity ligation assay at different time points over 42 days postradiosurgery. Results The expression of Notch1 and Notch4 receptors, Delta-like1, Delta-like4, Jagged1, and HES1 was observed in nidus vessels in the AVF rats pre- and postradiosurgery. Radiosurgery enhanced apoptotic activity (p < 0.05) and inhibited the expression of Notch1 and Notch4 receptors and Jagged1 in the endothelial cells of nidus vessels in the AVF rats at 1, 2, 3, 7, 21, 28, and 42 days postradiosurgery (p < 0.05). Radiosurgery suppressed the interaction events between Notch1 receptor and Jagged1 (p < 0.001) as well as Notch4 receptor and Jagged1 (p < 0.001) in the endothelial cells of nidus vessels in the AVF rats over a period of 42 days postradiosurgery. Radiosurgery induced thrombotic occlusion of nidus vessels in the AVF rats. There was a positive correlation between the percentage of fully obliterated nidus vessels and time after radiosurgery (r = 0.9324, p < 0.001). Conclusions Radiosurgery inhibits endothelial Notch1 and Notch4 signaling pathways in nidus vessels while inducing thrombotic occlusion of nidus vessels in a rat model of AVMs. The underlying mechanisms of radiosurgery-induced AVM shrinkage could be a combination of suppressing Notch receptor signaling in blood vessel endothelial cells, leading to a reduction in nidus vessel size and thrombotic occlusion of nidus vessels.
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Hadland, Brandon K., Barbara Varnum-Finney, Randall T. Moon, Michael Gustave Poulos, Jason M. Butler, Shahin Rafii, and Irwin D. Bernstein. "Notch Signaling By Either Notch1 or Notch2 Mediates Expansion of AGM-Derived Long-Term HSC Populations in Vitro." Blood 124, no. 21 (December 6, 2014): 2897. http://dx.doi.org/10.1182/blood.v124.21.2897.2897.

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Abstract Long-term, adult-engrafting hematopoietic stem cells (HSC) first emerge from hemogenic endothelial (HE) precursors in the context of embryonic arterial vessels such as the dorsal aorta of the AGM (Aorta-Gonad-Mesonephros region), a process which requires Notch1 receptor signaling. However, a possible subsequent role for Notch receptor activation during the unique period of substantial HSC expansion in embryonic development remains less well defined. Here, we show that endothelial cells derived from the murine embryonic AGM region (AGM-EC) or fetal liver (FL-EC) provide an in vitro substrate for generation/maturation of HSC from HE/HSC-precursor populations derived from early stage murine embryos, which lack adult-engraftment capacity prior to co-culture. Notably, these EC substrates, endogenously expressing Notch ligands of the Jagged and Delta families, also support subsequent numerical expansion of AGM-derived HSC, expressing Notch1 and Notch2 receptors, as determined by limit dilution transplantation analysis. Consistent with a requirement for Notch activation in this process, phenotypic HSC expansion during EC co-culture is blocked by gamma-secretase mediated Notch pathway inhibition. Furthermore, we show that in vitro Notch activation by immobilized ligand Delta1, together with cytokines and inhibition of the TGF-beta pathway, is sufficient to increase the number of AGM-derived HSC in the absence of EC stroma. Expansion of phenotypic hematopoietic stem/progenitor cells generated by culture on Delta1 is inhibited by antibody-mediated blockade of the combination of Notch1 and Notch2, but not by either Notch1 or Notch2 alone. Consistent with this, Notch receptor-specific activation by either immobilized Notch1 or Notch2 antibody is sufficient to support AGM-derived HSC in vitro in preliminary experiments. Altogether, these studies suggest a role for Notch pathway activation by either Notch1 or Notch2 in supporting embryonic-stage HSC expansion subsequent to initial Notch1-mediated HSC specification. Disclosures Moon: Fate Therapeutics: co-founder Other. Rafii:Angiocrine Biosciences: Founder Other.
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Urata, Yusuke, Wataru Saiki, Yohei Tsukamoto, Hiroaki Sago, Hideharu Hibi, Tetsuya Okajima, and Hideyuki Takeuchi. "Xylosyl Extension of O-Glucose Glycans on the Extracellular Domain of NOTCH1 and NOTCH2 Regulates Notch Cell Surface Trafficking." Cells 9, no. 5 (May 14, 2020): 1220. http://dx.doi.org/10.3390/cells9051220.

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Biochemical and genetic studies have indicated that O-linked glycosylation such as O-glucose (Glc), fucose (Fuc), and N-acetylglucosamine (GlcNAc) is critical for Notch signaling; however, it is not fully understood how O-glycans regulate the Notch receptor function. Notch receptors are type-I transmembrane proteins with large extracellular domains (ECD), containing 29–36 epidermal growth factor-like (EGF) repeats. Here, we analyzed O-Glc glycans on NOTCH1 and NOTCH2 expressed in HEK293T cells using an Orbitrap Fusion mass spectrometer and successfully revealed the structures and stoichiometries of all 17 EGF repeats of NOTCH1 with the O-Glc consensus sequence (C1-X-S-X-(P/A)-C2), and 16 out of 17 EGF repeats of NOTCH2 with the same consensus sequence. High levels of O-Glc attachment and xylosyl elongation were detected on most NOTCH1 and NOTCH2 EGF repeats. When both glucoside xylosyltransferases, GXYLT1 and GXYLT2, responsible for the xylosyl elongation of O-glucose, were genetically deleted, the expression of endogenous NOTCH1 and NOTCH2 on the surface of HEK293T cells did not change, but the cell surface expression of overexpressed NOTCH1 and NOTCH2 decreased compared with that in the wild type cells. In vitro secretion assays consistently showed a reduced secretion of both the NOTCH1 and NOTCH2 ECDs in GXYLT1 and GXYLT2 double knockout cells compared with the wild type cells, suggesting a significant role of the elongation of O-Glc glycans on the Notch ECDs in the quality control of Notch receptors.
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Demitrack, Elise S., Gail B. Gifford, Theresa M. Keeley, Nobukatsu Horita, Andrea Todisco, D. Kim Turgeon, Christian W. Siebel, and Linda C. Samuelson. "NOTCH1 and NOTCH2 regulate epithelial cell proliferation in mouse and human gastric corpus." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 2 (February 1, 2017): G133—G144. http://dx.doi.org/10.1152/ajpgi.00325.2016.

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The Notch signaling pathway is known to regulate stem cells and epithelial cell homeostasis in gastrointestinal tissues; however, Notch function in the corpus region of the stomach is poorly understood. In this study we examined the consequences of Notch inhibition and activation on cellular proliferation and differentiation and defined the specific Notch receptors functioning in the mouse and human corpus. Notch pathway activity was observed in the mouse corpus epithelium, and gene expression analysis revealed NOTCH1 and NOTCH2 to be the predominant Notch receptors in both mouse and human. Global Notch inhibition for 5 days reduced progenitor cell proliferation in the mouse corpus, as well as in organoids derived from mouse and human corpus tissue. Proliferation effects were mediated through both NOTCH1 and NOTCH2 receptors, as demonstrated by targeting each receptor alone or in combination with Notch receptor inhibitory antibodies. Analysis of differentiation by marker expression showed no change to the major cell lineages; however, there was a modest increase in the number of transitional cells coexpressing markers of mucous neck and chief cells. In contrast to reduced proliferation after pathway inhibition, Notch activation in the adult stomach resulted in increased proliferation coupled with reduced differentiation. These findings suggest that NOTCH1 and NOTCH2 signaling promotes progenitor cell proliferation in the mouse and human gastric corpus, which is consistent with previously defined roles for Notch in promoting stem and progenitor cell proliferation in the intestine and antral stomach. NEW & NOTEWORTHY Here we demonstrate that the Notch signaling pathway is essential for proliferation of stem cells in the mouse and human gastric corpus. We identify NOTCH1 and NOTCH2 as the predominant Notch receptors expressed in both mouse and human corpus and show that both receptors are required for corpus stem cell proliferation. We show that chronic Notch activation in corpus stem cells induces hyperproliferation and tissue hypertrophy, suggesting that Notch may drive gastric tumorigenesis.
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Pancewicz, J., and P. L. Bernatowicz. "Differential Notch1 and Notch2 expression in non-small cell lung cancer." Progress in Health Sciences 1 (June 11, 2019): 8–12. http://dx.doi.org/10.5604/01.3001.0013.3687.

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<b>Introduction:</b> NOTCH signaling can be deregulated in non-small cell lung cancer and can have oncogenic or tumor suppressive functions. NOTCH1 is regulated equally with NOTCH2, and the stability of the expression of those Notch receptors could determine the biological functions of lung cancer cells. <br/><b>Purpose:</b> To estimate expression level of NOTCH2 receptor in diverse NSCLC cell lines. Furthermore, we compared the mRNA level of NOTCH2 expression to the level of NOTCH1 expression. <br/><b>Materials and methods:</b> We have evaluated the mRNA manifestation of NOTCH1 and NOTCH2 genes by using quantitative real time method (RT-PCR). Moreover, we associated the results from NSCLC cells with results achieved in non-cancerous human bronchial epithelial cells (HBEpC). <br/><b>Results:</b> The expression level of NOTCH1 and NOTCH2 was downregulated in NSCLC cell lines, when related to HBEpC. Nevertheless, the decrease in NOTCH1 expression was significant, whereas NOTCH2 was not much different from the expression in control cells. <br/><b>Conclusions:</b> We conclude that NOTCH1 and NOTCH2 most likely have different biological function in NSCLC. They are active in NSCLC cell lines; nonetheless both are downregulated in lung cancer cells used in this study. Moreover, NOTCH2 expression is comparatively higher than NOTCH1 expression.
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Shi, Jianjun, Mohammad Fallahi, Jun-Li Luo, and Howard T. Petrie. "Nonoverlapping functions for Notch1 and Notch3 during murine steady-state thymic lymphopoiesis." Blood 118, no. 9 (September 1, 2011): 2511–19. http://dx.doi.org/10.1182/blood-2011-04-346726.

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Abstract Notch1 signaling is absolutely essential for steady-state thymic lymphopoiesis, but the role of other Notch receptors, and their potential overlap with the function of Notch1, remains unclear. Here we show that like Notch1, Notch3 is differentially expressed by progenitor thymocytes, peaking at the DN3 progenitor stage. Using mice carrying a gene-trapped allele, we show that thymic cellularity is slightly reduced in the absence of Notch3, although progression through the defined sequence of TCR-αβ development is normal, as are NKT and TCRγδ cell production. The absence of a profound effect from Notch3 deletion is not explained by residual function of the gene-trapped allele because insertion mapping suggests that the targeted allele would not encode functional signaling domains. We also show that although Notch1 and Notch3 are coexpressed on some early intrathymic progenitors, the relatively mild phenotype seen after Notch3 deletion does not result from the compensatory function of Notch1, nor does Notch3 function explain the likewise mild phenotype seen after conditional (intrathymic) deletion of Notch1. Our studies indicate that Notch1 and Notch3 carry out nonoverlapping functions during thymocyte differentiation, and that while Notch1 is absolutely required early in the lymphopoietic process, neither receptor is essential at later stages.
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Watanabe, Kazuhide, Tadahiro Nagaoka, Joseph M. Lee, Caterina Bianco, Monica Gonzales, Nadia P. Castro, Maria Cristina Rangel, et al. "Enhancement of Notch receptor maturation and signaling sensitivity by Cripto-1." Journal of Cell Biology 187, no. 3 (November 2, 2009): 343–53. http://dx.doi.org/10.1083/jcb.200905105.

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Nodal and Notch signaling pathways play essential roles in vertebrate development. Through a yeast two-hybrid screening, we identified Notch3 as a candidate binding partner of the Nodal coreceptor Cripto-1. Coimmunoprecipitation analysis confirmed the binding of Cripto-1 with all four mammalian Notch receptors. Deletion analyses revealed that the binding of Cripto-1 and Notch1 is mediated by the Cripto-1/FRL-1/Cryptic domain of Cripto-1 and the C-terminal region of epidermal growth factor–like repeats of Notch1. Binding of Cripto-1 to Notch1 occurred mainly in the endoplasmic reticulum–Golgi network. Cripto-1 expression resulted in the recruitment of Notch1 protein into lipid raft microdomains and enhancement of the furin-like protein convertase-mediated proteolytic maturation of Notch1 (S1 cleavage). Enhanced S1 cleavage resulted in the sensitization to ligand-induced activation of Notch signaling. In addition, knockdown of Cripto-1 expression in human and mouse embryonal carcinoma cells desensitized the ligand-induced Notch signaling activation. These results suggest a novel role of Cripto-1 in facilitating the posttranslational maturation of Notch receptors.
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Dissertations / Theses on the topic "Notch1 Receptor"

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Correia, Martins Vera Sofia. "Notch1 and Lymphotoxin beta receptor in thymopoiesis." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-56010.

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Liu, Zhaoli. "KLF4 regulates notch1 expression and signaling during epithelial transformation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2006. https://www.mhsl.uab.edu/dt/2008r/liu.pdf.

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Cullion, Kathleen J. "Mechanisms of NOTCH1 Mediated Leukemogenesis: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/537.

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Gain of function NOTCH1 mutations are common in both patients with T-ALL and in mouse models of the disease. Inhibiting the Notch pathway in T-ALL cell lines results in growth arrest and/or apoptosis in vitro, suggesting a requirement for Notch signaling in T-ALL. Therefore, we sought to examine the role of Notch1 signaling in both premalignancy and in the maintenance of leukemic growth. Using a murine model of T-ALL, in which expression of the Tal1 and Lmo2 oncogenes arrests thymocyte development, our preleukemic studies reveal that Notch1 mutations are early events that contribute to the clonal expansion of DN3 and DN4 progenitors. We also demonstrate that progenitors are maintained within the tumor and are enriched in leukemia-initiating cell (L-IC) activity, suggesting Notch1 may contribute to L-IC self-renewal. By studying the effects of Notch signaling in murine T-ALL cell lines, we also demonstrate that Notch1 promotes the proliferation and survival of leukemic blasts through regulation of Lef1 and the Akt/mTOR pathways. Given that T-ALL cell lines are dependent on Notch signaling in vitro, we investigated the effects of Notch inhibition in vivo. We provide evidence that Notch1 can be successfully targeted in vivo and that Notch inhibition, with γ-secretase inhibitors (GSIs), significantly extends the survival of leukemic mice. We also demonstrate that administration of GSIs in combination with rapamycin inhibits human T-ALL growth and extends survival in a mouse xenograft model. Given that NOTCH1 may be required to maintain both L-IC and bulk leukemic growth, targeting NOTCH1 may prove to be an efficacious targeted therapy for T-ALL patients with aberrant NOTCH1 activation.
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Chau, Dinh Le Mary. "Role of Notch1 in Cardiac Cell Differentiation and Migration: A Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/338.

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The cardiac conduction system is responsible for maintaining and orchestrating the rhythmic contractions of the heart. Results from lineage tracing studies indicate that precursor cells in the ventricles give rise to both cardiac muscle and conduction cells. Using chick embryonic hearts, we have found that Notch signaling plays an important role in the differentiation of cardiac muscle and conduction cell lineages in the ventricles. Notch1 expression coincides with a conduction marker at early stages of conduction system development. Mis-expression of constitutively active Notch1 (NIC) in early heart tubes exhibited multiple effects on cardiac cell differentiation. Cells expressing NIC had a significant decrease in the expression of cardiac muscle markers, but an increase in the expression of conduction cell markers. Loss-of-function studies further support that Notch1 signaling is important for the differentiation of these cardiac cell types. Functional electrophysiology studies show that the expression of constitutively active Notch1 resulted in abnormalities in ventricular conduction pathway patterns. During cardiogenesis, groups of myocardial cells become separated from each other, and migrate to form the trabeculae. These finger-like projections found within the ventricular chamber coalesce to generate the muscular portions of the interventricular septum, the thickened myocardium, and future sites of the conduction system. We have found that Notch signaling regulates the migration of cardiac cells during cardiogenesis. Over-expression of constitutively active Notch causes cells to localize more centrally within the heart, while loss-of-Notch function results in cells distributed within the periphery of the heart. Staining of heart sections shows that Notch signaling regulates the expression of N-cadherin, the predominant adhesion molecule in cardiomyocytes. We find that the effects of Notch on cell migration are two-fold: delamination and cell motility. Time-lapse studies demonstrate that Notch signaling increases cell motility, but does not affect speed or directionality of migration. Furthermore, we find that the effects of Notch on cell migration is independent of its effects on differentiation.
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Tesell, Jessica M. "The Notch1-c-Myc Pathway Mediates Leukemia-Initiating Cell Activity in Mouse T-ALL Models: A Dissertation." eScholarship@UMMS, 2013. http://escholarship.umassmed.edu/gsbs_diss/671.

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Although cure rates have significantly improved for children with T-cell acute lymphoblastic leukemia (T-ALL), 20-30% undergo induction failure or relapse with most succumbing to disease. Leukemia-initiating cells (L-ICs) are hypothesized to be resistant to conventional chemotherapy and radiation and are thereby responsible for disease recurrence. Using an in vivo limiting dilution assay, we previously showed that the murine T-ALL L-IC is quite rare, with only 0.003-0.05% of cells capable of initiating disease, and demonstrated that the L-IC is a subset of the leukemic DN3 thymic progenitor population. Work described in this thesis validates the L-IC assay using two transplantation methods to rule out effects of homing and/or microenvironment on T-ALL L-IC survival and maintenance. Using this assay, we demonstrate that sustained Notch1 signaling is required for T-ALL initiation in vivo and show that treatment with a Notch1 inhibitor reduces or in some cases eliminates the L-IC population. We further analyze the effects of inhibiting c-Myc, a Notch1-regulated gene, on L-IC frequency and uncover an essential role for c-Myc in L-IC survival and expansion. Suppressing c-Myc by using specific shRNAs or a c-Myc inhibitor reduces the L-IC population and interferes with leukemia initiation. Together, these findings reveal a critical role of the Notch1-c-Myc pathway in T-ALL initiation and suggest that therapeutics targeted at this pathway could be used to treat and/or prevent disease relapse in patients.
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Gómez, Martínez Valentí. "Noves funcions de Flotillin-1 en la regulació del procés de mitosi i la via de senyalització del receptor Notch1." Doctoral thesis, Universitat de Barcelona, 2009. http://hdl.handle.net/10803/1024.

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Flotillin-1 és una proteïna associada a membrana plasmàtica implicada en processos de trànsit de vesícules, reordenació del citoesquelet i transducció de senyals. Estudis previs en el laboratori han demostrat que Flotillin-1 és capaç de translocar-se a nucli en resposta a un estímul mitogènic i afavorir la proliferació de diverses línies cel·lulars. Els mecanismes mitjançant els quals provoca aquests efectes són desconeguts i objecte del present estudi.
D'una banda demostrem que Flotillin-1 és un factor regulador de la cinasa Aurora B, una proteïna que intervé en el control de la mitosi i més concretament en el anaphase checkpoint. El knock-down de Flotillin-1 provoca events mitòtics aberrants, acompanyats del descens tant en l'expressió d'Aurora B com de la seva activitat mesurada com els nivells de fosforilació de la histona H3. Flotillin-1 interacciona amb Aurora B i evita la seva degradació per la via del proteasoma.
D'altra banda, Flotillin-1 interacciona amb el receptor transmembrana Notch1, implicat en nombrosos processos de regulació de proliferació, diferenciació, apoptosi, etc. Flotillin-1 regula la localització subcel·lular de Notch1 així com la seva capacitat com activador transcripcional. La depleció o mutació de Flotillin-1 dificulta l'entrada de Notch1 a nucli i l'expressió dels gens diana de les famílies Hes/Hrt.
En conjunt, es presenta a Flotillin-1 com una proteïna capaç d'actuar a diferents nivells i regular processos i vies de senyalització cel·lular que li confereixen un paper com a regulador de la proliferació cel·lular.
Flotillin-1 is a protein associated to plasma membrane involved in vesicle trafficking, cyotskeleton reorganization and signal transduction. Previous findings in our laboratory has shown that Flotillin-1 is able to translocate the nucleus under mitogenic stimulus and increase proliferation rates of several cell lines. The mechanisms of action are unknown and object of the present study.
First, we show that Flotillin-1 is a regulator factor of the mitotic kinase Aurora B, a protein involved in control of mitosis and, specifically, in the anaphase checkpoint. The knock-down of Flotillin-1 causes aberrant mitotic events, decrease in Aurora B levels and its activity, measured as protein levels of phosporilated histone H3. Flotillin-1 interacts with Aurora B and avoid its degradation by the proteasome pathway.
In addition, Flotillin-1 interacts with the transmembrane receptor Notch1, involved in many regulatory processes of proliferation, differentiation, apoptosis, etc. Flotillin-1 regulates the subcellular localization of Notch1 and its activity as transcriptional activator. The mutation or depletion of Flotillin-1 difficult the entry of Notch1 in the nucleus and the expression of its target genes Hes/ HRT.
Overall, Flotillin-1 is a protein capable of acting at different levels, processes and signaling pathways in order to be a regulator of cell proliferation.
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Jotta, Patricia Yoshioka 1985. "Mutações de PTEN nas leucemias linfóides agudas T." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316892.

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Orientador: José Andres Yunes
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: A leucemia linfóide aguda (LLA) é o câncer mais frequente na infância, e destas, 15% são do tipo T (LLA-T). A hiperativação da via PI3K/Akt tem sido amplamente descrita em tumores e em linhagens celulares de LLA-T. PTEN é o principal regulador negativo dessa via e frequentemente encontra-se inativado em cânceres humanos. Com frequência, pacientes com LLA-T apresentam mutações ativadoras de NOTCH1. NOTCH1 pode regular transcricionalmente PTEN, contudo ainda não está claro como as mutações ativadoras de NOTCH1 influenciariam a expressão de PTEN nas LLA-T. Nós encontramos uma ocorrência de 11 (17,7%) mutações no éxon 7 do PTEN em 62 casos de LLA-T estudados consecutivamente. Contudo, nenhuma mutação foi encontrada na análise de 71 casos de LLA-B derivada. A maioria das mutações de PTEN apresentavam inserções/deleções de mais de 3 nucleotídeos. Não encontramos associação entre mutações em PTEN e o gênero, a idade e a contagem de glóbulos brancos ao diagnóstico. Pacientes com alterações no PTEN apresentaram uma tendência a pior sobrevida global (OS, p=0.07). Dentre os pacientes de LLA-T classificados como alto risco (n=56), aqueles possuindo anormalidades no PTEN mostraram-se associados significativamente a menor OS (p=0.019) e sobrevida livre de leucemia (LFS 47% vs 76%; p=0.045). As curvas de LFS foram significativamente diferentes (p=0.003), mesmo considerando apenas pacientes que atingiram a remissão no dia 28 do tratamento para a análise. Nosso estudo também mostrou que pacientes com mutações em NOTCH1 apresentavam aumento na transcrição de MYC e menor expressão de PTEN mRNA comparados a pacientes com NOTCH1 selvagem. Nós recentemente demonstramos que células de LLA-T apresentavam fosforilação de PTEN mediada por CK2, resultando na estabilização e consequentemente inativação da proteína PTEN. Corroborando ao estudo anterior, os casos de LLA-T analisados, independente do status de mutação em NOTCH1, expressam níveis significativamente mais altos de proteína PTEN do que controles normais. Para avaliar o impacto da regulação transcricional de NOTCH e a inativação postranscricional por CK2 de PTEN, nós tratamos as células de LLA-T com inibidores de gamma-secretase (DAPT e de CK2 (DRB/TBB). Nosso estudo enfatiza a relevância biológica e clínica da regulação do PTEN em LLA-T. E sugerimos o uso combinado de inibidores de gamma-secretase e CK2 devem possuir potencial terapêutico nas LLA-T
Abstract: T-cell acute lymphoblastic leukemia (T-ALL) accounts for approximately 15% of pediatric ALL. Patients with T-ALL are at increased risk of relapse compared with children treated for B-cell precursor ALL. Mutations in the phosphatase and tensin homolog (PTEN) gene leading to PTEN protein deletion and subsequent activation of the PI3K/Akt signaling pathway are common in cancer. PTEN is the main negative regulator of the PI3K/Akt survival pathway. T-ALL patients frequently display NOTCH1 activating mutations and Notch can transcriptionally down-regulate the tumor suppressor PTEN. However, it is not clear whether NOTCH1 mutations associate with decreased PTEN expression in primary T-ALL. We report that PTEN exon 7 mutations occurred in 11 (17.7%) out of 62 consecutive pediatric T-cell acute lymphoblastic leukemia (T-ALL) but in none of 71 precursor B-ALL patients. Most PTEN mutations were insertions/deletions of more than 3 nucleotides. No associations were found between PTEN mutation and age, gender, WBC at diagnosis, early response to therapy and remission rate. Patients with PTEN mutation (n=11) had a tendency toward worse overall survival (OS, p=0.07). Remarkably, PTEN mutations were significantly associated with lower OS (p=0.019) and leukemia-free survival (LFS 47% vs 76%, p=0.045) within patients classified in the high risk group (n=56). LFS curves were significantly different (p=0.003) even if only patients who reached remission on day 28 were considered for analysis. We compared patients with or without NOTCH1mutations and report that the former presented higher MYC transcript levels and decreased PTEN mRNA expression. We recently showed that T-ALL cells frequently display CK2-mediated PTEN phosphorylation, resulting in PTEN protein stabilization and concomitant functional inactivation. Accordingly, the T-ALL samples analyzed, irrespectively of their NOTCH1 mutational status, expressed significantly higher PTEN protein levels than normal controls. To evaluate the integrated functional impact of NOTCH transcriptional and CK2 post-translational inactivation of PTEN, we treated TALL cells with both the gamma-secretase inhibitor DAPT and the CK2 inhibitors DRB/TBB. Our data suggest that combined use of gamma-secretase and CK2 inhibitors may have therapeutic potential in T-ALL. And emphasize the biological and clinical relevance of PTEN regulation in pediatric T-ALL
Doutorado
Genetica Animal e Evolução
Doutor em Genetica e Biologia Molecular
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Baeten, Jeremy T. "The Roles of the Notch2 and Notch3 Receptors in Vascular Smooth Muscle Cells." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1480513055823902.

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Lee, Connie Wing-Ching. "Notch-1 and IGF-1 as Survivin Regulatory Pathways in Cancer: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/377.

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The 21st century brought about a dramatic increase in knowledge about genetic and molecular profiles of cancer. This information has validated the complexity of tumor cells and increased awareness of “nodal proteins”, but has yet to advance the development of rational targeted cancer therapeutics. Nodal proteins are critical cellular proteins that collect biological inputs and distribute the information across diverse biological processes. Survivin acts as a nodal protein by interfacing the multiple signals involved in mitosis and apoptosis and functionally integrate proliferation, cell death, and cellular homeostasis. By characterizing survivin as a target of both Type 1 Insulin-like Growth Factor (IGF-1) and Notch developmental signaling, we contribute to the paradigm of survivin as a nodal protein. The two signaling systems, Notch and IGF-1, regulate survivin by two independent mechanisms. Notch activation induces survivin transcription preferentially in basal breast cancer, a breast cancer subtype with poor prognosis and lack of molecular therapies. Activated Notch binds the transcription factor RBP-Jк and drives transcription from the survivin promoter. Notch mediated survivin expression increases cell cycle kinetics promoting tumor proliferation. Inhibition of Notch in a breast xenograft model reduced tumor growth and systemic metastasis. On the other hand, IGF-1 signaling drives survivin protein translation in prostate cancer cells. Binding of IGF-1 to its receptor activates downstream kinases, mammalian target of rapamycin (mTOR) and p70 S6 protein kinase (p70S6K), which modulates survivin mRNA translation to increase the apoptotic threshold. The multiple roles of survivin in tumorigenesis implicate survivin as a rational target for the “next generation” of cancer therapeutics.
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Karlström, Helena. "Notch receptor processing and CNS disease /." Stockholm : [Karolinska institutets bibl.], 2002. http://diss.kib.ki.se/2002/91-7349-300-7/.

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Books on the topic "Notch1 Receptor"

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Simpson, Pat. The notch receptors. Austin: R.G. Landes Co., 1994.

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Notch signaling: Methods and protocols. New York: Humana Press, 2014.

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Singh, Nita. The expression of the Notch receptors, Notch ligands, and the Fringe genes in hematopoiesis. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Kawakami, Toshiyuki. Cell differentiation of neoplastic cells originating in the oral and craniofacial regions. New York: Nova Science, 2008.

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Leow, Ching Ching. Genetic analysis of Notch receptor activation in mammary gland development. 2002.

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Cretegny, Kira. Expression of Notch receptors and ligands in lymphoid tissues. 2005.

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Notch Signaling In Embryology And Cancer. Springer, 2011.

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Notch Regulation Of The Immune System. Springer, 2012.

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Book chapters on the topic "Notch1 Receptor"

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González-García, Sara, Marina García-Peydró, Juan Alcain, and María L. Toribio. "Notch1 and IL-7 Receptor Signalling in Early T-cell Development and Leukaemia." In Current Topics in Microbiology and Immunology, 47–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/82_2012_231.

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Schnute, Björn, Tobias Troost, and Thomas Klein. "Endocytic Trafficking of the Notch Receptor." In Advances in Experimental Medicine and Biology, 99–122. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89512-3_6.

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Handford, Penny A., Boguslawa Korona, Richard Suckling, Christina Redfield, and Susan M. Lea. "Structural Insights into Notch Receptor-Ligand Interactions." In Advances in Experimental Medicine and Biology, 33–46. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89512-3_2.

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Bellavia, Diana, Saula Checquolo, Rocco Palermo, and Isabella Screpanti. "The Notch3 Receptor and Its Intracellular Signaling-Dependent Oncogenic Mechanisms." In Advances in Experimental Medicine and Biology, 205–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89512-3_10.

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Egan, S. E., B. St-Pierre, and C. C. Leow. "Notch Receptors, Partners and Regulators: From Conserved Domains to Powerful Functions." In Protein Modules in Signal Transduction, 273–324. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80481-6_11.

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Shah, Divya K., and Juan Carlos Zúñiga-Pflücker. "Notch Receptor-Ligand Interactions During T Cell Development, a Ligand Endocytosis-Driven Mechanism." In Current Topics in Microbiology and Immunology, 19–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/82_2012_225.

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Whiteman, Pat, Christina Redfield, and Penny A. Handford. "Bacterial Expression and In Vitro Refolding of Limited Fragments of the Notch Receptor and Its Ligands." In Methods in Molecular Biology, 193–208. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1139-4_15.

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"Other Transmembrane Receptor Classes: Signaling by TGF-β Receptors, TNF Receptors, Toll Receptors, and Notch." In Biochemistry of Signal Transduction and Regulation, 631–60. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2014. http://dx.doi.org/10.1002/9783527667475.ch14.

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Ahmed, Jessica. "Development of Specific Gamma Secretase Inhibitors." In Handbook of Research on Systems Biology Applications in Medicine, 423–37. IGI Global, 2009. http://dx.doi.org/10.4018/978-1-60566-076-9.ch025.

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Secretases are aspartic proteases, which specifically trim important, medically relevant targets such as the amyloid-precursor protein (APP) or the Notch-receptor. Therefore, changes in their activity can lead to dramatic diseases like M. Alzheimer caused by aggregation of peptidic fragments. On the other hand, the secretases are interesting targets for molecular therapy of the multiple myeloma, because the over-expressed Notch-receptor does not emerge into the native conformation until the cleavage by the presenilin, the active and catalytic subunit of the gamma secretase, occurs. Here, we focus on a novel methodology of structure-based drug development, feasible without prior knowledge of the target structure— analogy modeling. This combination of similarity screening, fold recognition, ligand-supported modeling, and docking is exemplarily illustrated for the structure of presenilin and specific inhibitors thereof.
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Sivaprakasam, Prathibha, Sureshkumar Anandasadagopan, Tamilselvi Alagumuthu, and Ashok Kumar Pandurangan. "Current Update on Natural Agents Against Triple Negative Breast Cancer." In Advanced Pharmacological Uses of Medicinal Plants and Natural Products, 91–113. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-2094-9.ch005.

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Breast cancer (BC) is sub-categorized into several well-recognized subtypes including estrogen receptor (ER), progesterone receptor (PR), and HER2 triple-negative breast cancer (TNBC). It is a heterogeneous disease entity constituting about 15% of breast cancer cases worldwide. TNBC is associated with poor prognosis and lack of sustained response to conventional chemotherapeutic agents. Although no approved targeted therapy is available for TNBCs, molecular-profiling efforts have revealed promising molecular targets such as the Wnt/β-catenin, STAT3, VEGF, EGFR, polyadenosine ribose polymerase inhibitors (PARPi) and DNA repair pathway, androgen pathway, and NOTCH pathway. Moreover, more research needs to be performed in the area of TNBC aiming at dissecting potential pathways and identifying potential molecular signatures to develop new targeted biologic modifiers. Natural agents are the abundant chemical compounds available from diverse plants. The authors aimed to summarize the current evidence and discuss the natural agents that target TNBC using different pathways.
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Conference papers on the topic "Notch1 Receptor"

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Monticone, Giulia, Fokhrul M. Hossain, Deniz A. Ucar, Samarpan Majumder, Claudia Sorrentino, Paulo C. Rodriguez, Rosa A. Sierra, et al. "Abstract 4517: Targeting Notch1 via adenosine A2A receptor to modulate tumor immunity." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4517.

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Pohlmann, Elliot, Susan Murphy, Debbie Kelly, and Zhi Sheng. "Abstract 3862: Isolation and nanoscale visualization of glioblastoma stem-like cells utilizing the Notch1 receptor." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3862.

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Olayinka, Abidemi, Eoin Corcoran, Brendan O’Connor, and Paul A. Cahill. "11 The role of N-glycosylation of the NOTCH1 receptor in jagged1-stimulated myogenic differentiation in vitro." In The Scottish Cardiovascular Forum 2018, 3rd February 2018, Trinity Biomedical Science Institute, Trinity College Dublin Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-scf.21.

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Psyrri, Amanda, Eirini Pectasides, M. Avgeris, Apostolos Klinakis, Andreas Scorilas, Clarence Sasaki, George Fountzilas, and Theodoros Rampias. "Abstract A183: Identification of an exon 31-deletion variant of Notch1 receptor with frequent expression in head and neck cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a183.

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Zehender, H., E. C. Witte, K. Stegemeier, and A. Patscheke. "IRREVERSIBLE BLOCKADE OF THE THROMBOXANE A2/PROSTAGLANDIN H2 RECEPTOR OF HUMAN PLATELETS BY AZIDO-BSP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643755.

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Azido-BSP (4-[2-(4-azido-benzenesulphonylamino)-ethyl]phen-oxyacetic acid) is a photolabile derivative of the competitive thromboxane A2 /prostaglandin H2 (TXA2/PGH2) receptor antagonist sulotroban (=BM 13.177). If protected from short wave light, azido-BSP reversibly inhibited the platelet shape change induced by the PGH2 analogue U 46619 but notthe shape change induced by ADP or PAF. Schild analysis revealed an apparent KD=0.2 μM with washed platelets. The irreversible inhibition requiredirradiation of the platelet suspensionwith UVlight (254 nm) for 5 minutes in the presenceof azido-BSP. After this treatment,the platelets were washed twice and used forplatelet function tests. Treatment with 0.5 μM of azido-BSP suppressed the U 46619(10 μM)-induced (3H)serotonin release and 1 μM of azido-BSP was necessary to block the U 46619(2 μM)-inducedaggregation.The platelet shape change induced by U 46619 (0.01μM) was only partially inhibited, even at very high concentrations (50μM) of the antagonist.This suggests that a small portion of the TXA2/PGH2 receptors could not be blocked bythe photoaffinity treatment with azido-BSP. After treatment with 1 μM azido-BSP, the shape change stimulated by ADP or PAF was not reduced. This indicates a high specificity of thephotoaffinity ligand for the TXA2/PGH2 receptor. It is concluded that UV irradiation of azido-BSP generates anitrene intermediate that covalently links to the majority of the TXA2/PGH2 receptors. Azido-BSP provides a specific tool for tagging and subsequent purification of the TXA2/PGH2 receptor of platelets.(Supported by the Deutsche Forschungsgemeinschaft, Grant Pa263).
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Wallace, Breanna, Min Wang, Chris Muriel, Jennifer Cain, Belinda Cancilla, Jalpa Shah, Jie Wei, et al. "Abstract 213: Novel NOTCH3 activating mutations identified in tumors sensitive to OMP-59R5, a monoclonal antibody targeting the Notch2 and Notch3 receptors." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-213.

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Cancilla, Belinda, Wan-Ching Yen, Chun Zhang, Marcus M. Fischer, May Ji, Tracy Tang, Yu-Wang Liu, et al. "Abstract 910: NOTCH3 expression is predictive of efficacy in pancreas tumor models treated with OMP-59R5, a monoclonal antibody targeting the NOTCH2 and NOTCH3 receptors." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-910.

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Bell, Alisa, Heidi Okamura, David Keane, Samantha Perino, Jeanine Lorusso, Jeno Gyuris, and Ronan O'Hagan. "Abstract A73: Understanding specificity in Notch receptor signaling." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-a73.

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Geles, Kenneth G., Yijie Gao, Latha Sridharan, Andreas Giannakou, Ting-Ting Yamin, Jonathan Golas, Judy Lucas, et al. "Abstract 1697: Therapeutic targeting the NOTCH3 receptor with antibody drug conjugates." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1697.

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Okamura, Heidi, Jeanine Lorusso, Alisa Bell, Samantha Perino, David Keane, Joelle Brodeur, Adrian Cooper, et al. "Abstract 5170: Monoclonal antibodies to Notch receptors inhibit tumor maintenance." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5170.

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Reports on the topic "Notch1 Receptor"

1

Kitajewski, Jan K. Role of Notch/VEGF-Receptor 3 in Breast Tumor Angiogenesis and Lymphangiogenesis. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada446379.

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Kitajewski, Jan K. Role of Notch/VEGF-Receptor 3 in Breast Tumor Angiogenesis and Lymphangiogenesis. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada475616.

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