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Academic literature on the topic 'P75NTR'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "P75NTR"

1

Franco, María Luisa, Irmina García-Carpio, Raquel Comaposada-Baró, Juan J. Escribano-Saiz, Lucía Chávez-Gutiérrez, and Marçal Vilar. "TrkA-mediated endocytosis of p75-CTF prevents cholinergic neuron death upon γ-secretase inhibition." Life Science Alliance 4, no. 4 (February 3, 2021): e202000844. http://dx.doi.org/10.26508/lsa.202000844.

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γ-secretase inhibitors (GSI) were developed to reduce the generation of Aβ peptide to find new Alzheimer’s disease treatments. Clinical trials on Alzheimer’s disease patients, however, showed several side effects that worsened the cognitive symptoms of the treated patients. The observed side effects were partially attributed to Notch signaling. However, the effect on other γ-secretase substrates, such as the p75 neurotrophin receptor (p75NTR) has not been studied in detail. p75NTR is highly expressed in the basal forebrain cholinergic neurons (BFCNs) during all life. Here, we show that GSI treatment induces the oligomerization of p75CTF leading to the cell death of BFCNs, and that this event is dependent on TrkA activity. The oligomerization of p75CTF requires an intact cholesterol recognition sequence (CRAC) and the constitutive binding of TRAF6, which activates the JNK and p38 pathways. Remarkably, TrkA rescues from cell death by a mechanism involving the endocytosis of p75CTF. These results suggest that the inhibition of γ-secretase activity in aged patients, where the expression of TrkA in the BFCNs is already reduced, could accelerate cholinergic dysfunction and promote neurodegeneration.
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Marchetti, Laura, Fulvio Bonsignore, Francesco Gobbo, Rosy Amodeo, Mariantonietta Calvello, Ajesh Jacob, Giovanni Signore, et al. "Fast-diffusing p75NTR monomers support apoptosis and growth cone collapse by neurotrophin ligands." Proceedings of the National Academy of Sciences 116, no. 43 (September 12, 2019): 21563–72. http://dx.doi.org/10.1073/pnas.1902790116.

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The p75 neurotrophin (NT) receptor (p75NTR) plays a crucial role in balancing survival-versus-death decisions in the nervous system. Yet, despite 2 decades of structural and biochemical studies, a comprehensive, accepted model for p75NTR activation by NT ligands is still missing. Here, we present a single-molecule study of membrane p75NTR in living cells, demonstrating that the vast majority of receptors are monomers before and after NT activation. Interestingly, the stoichiometry and diffusion properties of the wild-type (wt) p75NTR are almost identical to those of a receptor mutant lacking residues previously believed to induce oligomerization. The wt p75NTR and mutated (mut) p75NTR differ in their partitioning in cholesterol-rich membrane regions upon nerve growth factor (NGF) stimulation: We argue that this is the origin of the ability of wt p75NTR , but not of mut p75NTR, to mediate immature NT (proNT)-induced apoptosis. Both p75NTR forms support proNT-induced growth cone retraction: We show that receptor surface accumulation is the driving force for cone collapse. Overall, our data unveil the multifaceted activity of the p75NTR monomer and let us provide a coherent interpretative frame of existing conflicting data in the literature.
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Klinger, Mary Beth, and Margaret A. Vizzard. "Role of p75NTR in female rat urinary bladder with cyclophosphamide-induced cystitis." American Journal of Physiology-Renal Physiology 295, no. 6 (December 2008): F1778—F1789. http://dx.doi.org/10.1152/ajprenal.90501.2008.

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Previous studies demonstrated changes in urinary bladder neurotrophin content and upregulation of neurotrophin receptors, TrkA and the p75 neurotrophin receptor (p75NTR), in micturition reflex pathways after cyclophosphamide (CYP)-induced cystitis. p75NTR can bind nerve growth factor (NGF) and modulate NGF-TrkA binding and signaling. We examined p75NTR expression and the role of p75NTR in the micturition reflex in control and CYP-treated rats. p75NTR Immunoreactivity was present throughout the urinary bladder. CYP-induced cystitis (4 h, 48 h, chronic) increased ( P ≤ 0.05) p75NTR expression in whole urinary bladder as shown by Western blotting. The role of p75NTR in bladder function in control and CYP-treated rats was determined using conscious cystometry and immunoneutralization or PD90780, a compound known to specifically block NGF binding to p75NTR. An anti-p75NTR monoclonal antibody or PD90780 was infused intravesically and cystometric parameters were evaluated. Both methods of p75NTR blockade significantly ( P ≤ 0.05) decreased the intercontraction interval and void volume in control and CYP-treated rats. Intravesical infusion of PD90780 also significantly ( P ≤ 0.001) increased intravesical pressure and increased the number of nonvoiding contractions during the filling phase. Control intravesical infusions of isotype-matched IgG and vehicle were without effect. Intravesical instillation of PD90780 significantly ( P ≤ 0.01) reduced the volume threshold to elicit a micturition contraction in control rats (no inflammation) and CYP-treated in a closed urinary bladder system. These studies demonstrate 1) ubiquitous p75NTR expression in urinary bladder and increased expression with CYP-induced cystitis and 2) p75NTR blockade at the level of the urinary bladder produces bladder hyperreflexia in control and CYP-treated rats. The overall activity of the urinary bladder reflects the balance of NGF-p75NTR and NGF-TrkA signaling.
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Tan, Wei, Longjia Dong, Xuexing Shi, Qian Tang, and Dianming Jiang. "P75NTR Exacerbates SCI-induced Mitochondrial Damage and Neuronal Apoptosis Depending on NTRK3." Current Neurovascular Research 18, no. 5 (October 2021): 552–64. http://dx.doi.org/10.2174/1567202619666211231091834.

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Objective: The aim of the study was to investigate the mechanism by which p75 neurotrophin receptor (p75NTR) affects mitochondrial damage and neuronal apoptosis in spinal cord injury (SCI). Methods: After the establishment of SCI rat models, short hairpin (sh) RNA of p75NTR and control sh-RNA were injected into SCI rats, respectively. On days 1, 7 and 21 after SCI, the severity of SCI and cell apoptosis in SCI rats were determined as well as the recovery of hind limb performance and p75NTR expression. After spinal cord neurons were transfected with p75NTR overexpression plasmid or empty plasmid vector or cotransfected with overexpression plasmids of p75NTR and neurotrophic tyrosine receptor kinase3 (NTRK3), the expression levels of p75NTR and NTRK3 were quantified. Moreover, we detected the apoptosis and proliferation rates of the neurons in addition to the levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) in the neurons. The binding between p75NTR and NTRK3 was confirmed via Co-immunoprecipitation (Co-IP). Results: The rat spinal cords in the Model group were notably damaged after SCI accompanied by increased apoptosis and decreased locomotor function. The expression of p75NTR was significantly upregulated after SCI. The aforementioned injuries were remarkably ameliorated in response to injection of sh-p75NTR. p75NTR overexpression induced mitochondrial damage and neuronal apoptosis in spinal cord neurons, while the promotive effects were perturbed by NTRK3 overexpression. Furthermore, p75NTR directly bound to and downregulated NTRK3. Conclusion: Both in vivo and in vitro experiments showed that p75NTR aggravates mitochondrial damage and neuronal apoptosis in SCI through downregulating NTRK3.
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Kenchappa, Rajappa, and Peter A. J. Forsyth. "Relationship of the p75 neurotrophin receptor (p75NTR) and hypoxic response and treatment resistance in malignant gliomas." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e13026-e13026. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e13026.

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e13026 Background: Malignant gliomas (MGs) are resistant to Radiotherapy (RT). The molecular pathways that produce resistance to therapy and ability to tolerate hypoxia are poorly understood. We previously found that the p75NTR causes invasion & proliferation of MGs/Brain Tumor Initiating Cells (BTICs). We think MGs use the neurotrophin-rich brain environment as a survival advantage to resist treatment by expressing the p75NTR. We hypothesize that hypoxia cause p75NTR proteolysis which produces HIF-1α stabilization and activation of hypoxic responses. This repertoire of hypoxic responses leads to resistance to both hypoxia & radiotherapy (RT) and account for MG recurrence. Methods: We used glioma cells and BTICs they express very low or and high levels of p75NTR and manipulated the expression of p75NTR by shRNAs and activation by mutant receptors and pharmacological inhibitors. We exposed these cells to hypoxia and radiation treatment and performed biochemical and functional assays. We have also used paired pre and post-RT frozen patient specimens. Gene expression profiles were analyzed for patients using microarray expression data for 516 primary GBM patients from the TCGA and 239 patients from Moffitt’s Total Cancer Care (TCC) project. Results: We found that inhibiting p75NTR pharmacologically significantly reduced invasion/proliferation of MGs/BTICs in vitro & in vivo. We have also found that p75NTR is required for HIF-1α stabilization and VEGF expression in MGs/BTICs in vitro & in vivo, that p75NTR expressing MGs/BTICs are very resistant to hypoxia & RT in vitro, and these effects are reversed with inhibition of p75NTR signaling. In addition, p75NTR expression and its cleavage are associated with treatment resistance in patient specimens. We also found using TCGA and Moffitt patient specimen data that the p75NTR/Siah2/PHD axis is expressed in MG patients and associated with RT resistance/poor prognosis. Conclusions: These results suggest that p75NTR expression/cleavage are required for HIF-1α pathway activation and hence the phenotype of MGs/BTICs and their treatment resistance. Targeting the p75NTR signaling axis therefore will provide novel therapeutic approaches.
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Barrio, Tomás, Enric Vidal, Marina Betancor, Alicia Otero, Inmaculada Martín-Burriel, Marta Monzón, Eva Monleón, Martí Pumarola, Juan José Badiola, and Rosa Bolea. "Evidence of p75 Neurotrophin Receptor Involvement in the Central Nervous System Pathogenesis of Classical Scrapie in Sheep and a Transgenic Mouse Model." International Journal of Molecular Sciences 22, no. 5 (March 8, 2021): 2714. http://dx.doi.org/10.3390/ijms22052714.

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Neurotrophins constitute a group of growth factor that exerts important functions in the nervous system of vertebrates. They act through two classes of transmembrane receptors: tyrosine-kinase receptors and the p75 neurotrophin receptor (p75NTR). The activation of p75NTR can favor cell survival or apoptosis depending on diverse factors. Several studies evidenced a link between p75NTR and the pathogenesis of prion diseases. In this study, we investigated the distribution of several neurotrophins and their receptors, including p75NTR, in the brain of naturally scrapie-affected sheep and experimentally infected ovinized transgenic mice and its correlation with other markers of prion disease. No evident changes in infected mice or sheep were observed regarding neurotrophins and their receptors except for the immunohistochemistry against p75NTR. Infected mice showed higher abundance of p75NTR immunostained cells than their non-infected counterparts. The astrocytic labeling correlated with other neuropathological alterations of prion disease. Confocal microscopy demonstrated the co-localization of p75NTR and the astrocytic marker GFAP, suggesting an involvement of astrocytes in p75NTR-mediated neurodegeneration. In contrast, p75NTR staining in sheep lacked astrocytic labeling. However, digital image analyses revealed increased labeling intensities in preclinical sheep compared with non-infected and terminal sheep in several brain nuclei. This suggests that this receptor is overexpressed in early stages of prion-related neurodegeneration in sheep. Our results confirm a role of p75NTR in the pathogenesis of classical ovine scrapie in both the natural host and in an experimental transgenic mouse model.
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Majdan, Marta, Gregory S. Walsh, Raquel Aloyz, and Freda D. Miller. "TrkA mediates developmental sympathetic neuron survival in vivo by silencing an ongoing p75NTR-mediated death signal." Journal of Cell Biology 155, no. 7 (December 24, 2001): 1275–86. http://dx.doi.org/10.1083/jcb.200110017.

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Developmental sympathetic neuron death is determined by functional interactions between the TrkA/NGF receptor and the p75 neurotrophin receptor (p75NTR). A key question is whether p75NTR promotes apoptosis by directly inhibiting or modulating TrkA activity, or by stimulating cell death independently of TrkA. Here we provide evidence for the latter model. Specifically, experiments presented here demonstrate that the presence or absence of p75NTR does not alter Trk activity or NGF- and NT-3–mediated downstream survival signaling in primary neurons. Crosses of p75NTR−/− and TrkA−/− mice indicate that the coincident absence of p75NTR substantially rescues TrkA−/− sympathetic neurons from developmental death in vivo. Thus, p75NTR induces death regardless of the presence or absence of TrkA expression. These data therefore support a model where developing sympathetic neurons are “destined to die” by an ongoing p75NTR-mediated apoptotic signal, and one of the major ways that TrkA promotes neuronal survival is by silencing this ongoing death signal.
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Yang, Yaoli Pu, Simeng Wang, Xingguo Li, and Nina F. Schor. "Cell Line-Dependent Variability of Coordinate Expression of p75NTR and CRABP1 and Modulation of Effects of Fenretinide on Neuroblastoma Cells." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/7568287.

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Neuroblastoma is a childhood neural crest tumor. Fenretinide, a retinoic acid analogue, induces accumulation of mitochondrial reactive oxygen species and consequent apoptosis in neuroblastoma cells. The p75 neurotrophin receptor (p75NTR) enhances the antineuroblastoma cell efficacy of fenretinidein vitro. We examined the role of the retinoid binding protein, CRABP1, in p75NTR-mediated potentiation of the efficacy of fenretinide. Knockdown and overexpression, respectively, of either p75NTR or CRABP1 were effected in neuroblastoma cell lines using standard techniques. Expression was determined by qRT-PCR and confirmed at the protein level by Western blot. Metabolic viability was determined by Alamar blue assay. While protein content of CRABP1 correlated roughly with that of p75NTR in the three neuroblastoid or epithelioid human neuroblastoma cell lines studied, manipulation of p75NTR expression resulted in cell line-dependent, variable change in CRABP1 expression. Furthermore, in some cell lines, induced expression of CRABP1 in the absence of p75NTR did not alter cell sensitivity to fenretinide treatment. The effects of manipulation of p75NTR expression on CRABP1 expression and the effects of CRABP1 expression on fenretinide efficacy are therefore neuroblastoma cell line-dependent. Potentiation of the antineuroblastoma cell effects of fenretinide by p75NTR is not mediated solely through CRABP1.
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Triaca, Viviana, Elena Fico, Pamela Rosso, Massimo Ralli, Alessandro Corsi, Cinzia Severini, Alvaro Crevenna, et al. "Pilot Investigation on p75ICD Expression in Laryngeal Squamous Cell Carcinoma." Cancers 14, no. 11 (May 25, 2022): 2622. http://dx.doi.org/10.3390/cancers14112622.

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We investigated the p75 Neurotrophin Receptor (p75NTR) expression and cleavage product p75NTR Intracellular Domain (p75ICD) as potential oncogenic and metastatic markers in human Laryngeal Squamous Cell Carcinoma (LSCC). p75NTR is highly expressed in Cancer Stem Cells (CSCs) of the laryngeal epithelia and it has been proposed as a marker for stemness, cell migration, and chemo-resistance in different squamous carcinomas. To investigate the clinical significance of p75NTR cleavage products in solid tumors, full-length and cleaved p75NTR expression was analyzed in laryngeal primary tumors from different-stage LSCC patients, diagnosed at the Policlinico Umberto I Hospital. Molecular and histological techniques were used to detect the expressions of p75NTR and p75ICD, and ATP Binding Cassette Subfamily G Member 2 (ABCG2), a CSC marker. We found regulated p75NTR cleavage during squamous epithelial tumor progression and tissue invasion. Our preliminary investigation suggests p75ICD expression and localization as possible features of tumorigenesis and metastaticity. Its co-localization with ABCG2 in squamous cells in the parenchyma invaded by the tumor formation allows us to hypothesize p75NTR and p75ICD roles in tumor invasion and CSC spreading in LSCC patients. These data might represent a starting point for a comprehensive analysis of p75NTR cleavage and of its clinical relevance as a potential molecular LSCC signature, possibly helping diagnosis, and improving prognosis and personalized therapy.
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Tuffereau, Christine, Klaus Schmidt, Christelle Langevin, Florence Lafay, Georg Dechant, and Martin Koltzenburg. "The Rabies Virus Glycoprotein Receptor p75NTR Is Not Essential for Rabies Virus Infection." Journal of Virology 81, no. 24 (October 10, 2007): 13622–30. http://dx.doi.org/10.1128/jvi.02368-06.

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ABSTRACT Rabies virus glycoprotein (RVG) is known to be the only factor that mediates rabies infection. The neurotrophin receptor (p75NTR), through its cysteine-rich domain 1, is a specific receptor for RVG and neutralizes virus infectivity, but its role in virus infection has remained obscure. We used adult mouse dorsal root ganglion (DRG) neurons as a model to study the role of p75NTR in RV infection of primary neurons. We show that RV infects around 20% of DRG neurons, of which more than 80% are p75NTR positive, have large diameters, and are capsaicin insensitive. Surprisingly, RV binding and infection are absent in about half of the p75NTR-expressing DRG neurons which have small diameters and are often capsaicin sensitive. This indicates that p75NTR is not sufficient to mediate RV interaction in sensory neurons. The rate and specificity of neural infection are unchanged in RV-infected p75NTRExonIV−/− mice that lack all extracellular receptor domains and in wild-type mice infected with two independent RV mutants that lack p75NTR binding. Accordingly, the mortality rate is unchanged in the absence of RV-p75NTR interaction. We conclude that although p75NTR is a receptor for soluble RVG in transfected cells of heterologous expression systems, an RVG-p75NTR interaction is not necessary for RV infection of primary neurons. This means that other receptors are required to mediate RV infection in vivo and in vitro.
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Dissertations / Theses on the topic "P75NTR"

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Paul, Christine E. "Analysis of p75NTR-dependent apoptotic pathways and of p75NTR gene products." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19468.

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The p75 neurotrophin receptor (p75NTR) binds members of the neurotrophin family and plays important roles in the regulation of neuronal survival, apoptosis and growth during development and after nervous system injury. Many in vitro and in vivo studies have shown that p75NTR induces cell death, though the signaling events that link p75NTR activation to apoptosis are not thoroughly understood. p75NTR-dependent apoptosis is associated with an increase in Rac and Jun kinase (JNK) activity, and recent work from our laboratory has shown that the p75NTR interactor, NRAGE, activates a mitochondrial death pathway involving JNK-dependent cytochrome C release and activation of Caspase-9, Caspase-7 and Caspase-3. Despite this progress, several important details of p75NTR apoptotic signaling remain unknown. In particular, it is unclear what targets of p75NTR-dependent JNK activation result in mitochondrial cytochrome C release and caspase activation. BH3-domain-only proteins are members of the Bcl-2 family that induce the association of Bax and Bak which in turn facilitate release of mitochondrial proteins such as cytochrome C into the cytosol. Transcriptional activation of BH3-domain-only genes through c-Jun- or p53-dependent pathways is implicated in apoptosis in neuronal and non-neuronal systems. In the first part of this thesis, I examined whether p75NTR-induced apoptosis is correlated with accumulation of BH3-domain-only gene products. U373 human glioma cells and mouse cortical neurons were infected with adenovirus expressing p75NTR to constitutively activate p75NTR-dependent pathways, and alterations in mRNA levels of the BH3-domain-only family members Bim, Bmf, Hrk, Bik, Puma, and Noxa were determined by RT-PCR. The results from these experiments showed that p75NTRmediated cell death did not result in BH3-domain-only gene transcription. Subsequent studies in our laboratory established that the BH3-domain-only protein, Bad, is phosphorylated on Serine 128 in a JNK-dependent manner, and that this phosphorylation is a critical component of p75NTR-dependent apoptosis. The generation of animals that lack p75NTR expression has been a critical advance in understanding the in vivo role of this receptor. In the second part of this thesis, I analyzed the recently created p75NTRExonlv-/- mice, which were shown to produce a null mouse lacking all p75NTR gene products, in contrast to the previously constructed p75NTRExon1"-/- mouse, which maintains expression of an alternatively spliced form of p75NTR (s-p75NTR). Our studies revealed that 75NTRExonIV-/- mice continue to express a p75NTR gene product that encodes a truncated protein containing the p75NTR extracellular stalk region together with the entire transmembrane and intracellular domains. The gene product is initiated from a cryptic Kozak consensus/initiator ATG sequence within a region of Exon IV located 3' to the pGK-Neo insertion site, likely as a result of enhancer elements within pGK-Neo cassette. Characterization of this protein product indicated that it localized to the plasma membrane and overexpression of the p75NTRExonIV fragment in heterologous cells resulted in activation of JNK and cleavage of Procaspase 3, indicating that it can mediate pro-apoptotic effects in vivo. These results indicate that aspects of the p75NTRExonIV-/- phenotype may reflect a gain-of-function mutation rather than a loss of p75NTR function.
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Kanning, Kevin C. "Characterization of the p75NTR/NRH subfamily /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/10665.

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Hucho, Tim. "Der Neurotrophinrezeptor p75NTR eine biochemische Untersuchung /." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/115/index.html.

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Schweigreiter, Rüdiger. "Untersuchungen über die funktionelle Rolle des Neurotrophinrezeptors p75NTR." Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-8187.

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Bandoła, Joanna, Cornelia Richter, Martin Ryser, Arshad Jamal, Michelle P. Ashton, Bonin Malte von, Matthias Kuhn, et al. "Neurotrophin Receptor p75NTR Regulates Immune Function of Plasmacytoid Dendritic Cells." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-230813.

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Plasmacytoid dendritic cells (pDCs) regulate innate and adaptive immunity. Neurotrophins and their receptors control the function of neuronal tissue. In addition, they have been demonstrated to be part of the immune response but little is known about the effector immune cells involved. We report, for the first time, the expression and immune-regulatory function of the low affinity neurotrophin receptor p75 neurotrophin receptor (p75NTR) by the antigen-presenting pDCs, mediated by toll-like receptor (TLR) 9 activation and differential phosphorylation of interferon regulatory factor 3 and 7. The modulation of p75NTR on pDCs significantly influences disease progression of asthma in an ovalbumin-induced mouse model mediated by the TLR9 signaling pathway. p75NTR activation of pDCs from patients with asthma increased allergen-specific T cell proliferation and cytokine secretion in nerve growth factor concentration-dependent manner. Further, p75NTR activation of pDCs delayed the onset of autoimmune diabetes in RIP-CD80GP mice and aggravated graft-versus-host disease in a xenotransplantation model. Thus, p75NTR signaling on pDCs constitutes a new and critical mechanism connecting neurotrophin signaling and immune response regulation with great therapeutic potential for a variety of immune disorders.
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Wilmet, Jean-Philippe. "Etude proteomique du recepteur p75NTR dans le cancer du sein." Thesis, Lille 1, 2011. http://www.theses.fr/2011LIL10060/document.

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Le facteur de croissance neurotrophique NGF (Nerve Growth Factor) est un facteur mitogène et de survie pour les cellules de cancer du sein alors qu’il est sans effet sur la croissance des cellules épithéliales mammaires normales. Ce facteur de croissance agit sur ses cellules cibles par l’intermédiaire de deux récepteurs : TrkA, qui est un récepteur tyrosine kinase, et p75NTR, dépourvu d’activité catalytique intrinsèque. Le NGF stimule la survie des cellules cancéreuses mammaires via p75NTR en activant le facteur de transcription NF-ĸB. Au cours de mes travaux de thèse, je me suis tout d’abord appliqué à décrire les modifications du protéome induites par une surexpression de ce récepteur p75NTR. Pour cela, nous avons établi une lignée cellulaire MCF-7 surexprimant stablement le récepteur p75NTR. Par la suite, une étude par électrophorèse bidimensionnelle suivie par une analyse par spectrométrie de masse de type MALDI-TOF/TOF a été réalisée en comparant des cellules non stressées à des cellules induites en apoptose grâce à l’apoptogène TRAIL (TNF-related-apoptosis-inducing-ligand). Au cours de cette étude, nous avons pu mettre en évidence un certain nombre de protéines régulées par la présence de p75NTR en condition d’apoptose comme les cytokératines 8, 18 et 19, la protéine chaperonne HSP27 ou bien encore la protéine ribosomale RPLP0. Ces résultats suggèrent l’importance d’une réorganisation de ces protéines afin que p75NTR puisse effectuer son effet de survie. L’autre partie de mes travaux a consisté en une étude spécifique des partenaires de signalisation de p75NTR. Pour ce faire, nous avons décidé d’appliquer la stratégie TAP-Tag (Tandem Affinity Purification-Tag), une approche de protéomique fonctionnelle, au récepteur membranaire p75NTR. Une analyse différentielle de plusieurs conditions de culture par spectrométrie de masse de type nanoLC-MS/MS a abouti à l’obtention d’une liste de partenaires potentiels de signalisation de p75NTR dans un contexte de survie cellulaire. Cependant, l’implication fonctionnelle de ces protéines doit être confirmée. L’ensemble de ces travaux a permis d’ouvrir de nouvelles pistes de recherche pour comprendre à la fois les mécanismes cellulaires mis en œuvre lors de la survie des cellules cancéreuses mammaires, mais aussi les partenaires potentiels de signalisation du récepteur p75NTR
The growth factor NGF (nerve growth factor) is a mitogenic and survival factor for breast cancer cells but has no effect on normal epithelial mammary cell growth. This growth factor acts on breast cancer cells via two receptors : TrkA, a tyrosine kinase receptor, and p75NTR, which has no catalytic activity. NGF promotes breast cancer cells survival via p75NTR by activation of the transcriptional factor NF-κB. In the first time of my thesis work, I have described the proteome modification induced by an overexpression of p75NTR in apoptotic stress-induced breast cancer cells. We established a p75NTR overexpressing MCF-7 cell line. Thus, we investigated, by two dimensional electrophoresis followed by MALDI-TOF/TOF based mass spectrometry analysis, the proteome modification induced by the pro-apoptotic agent TRAIL (TNF-related-apoptosis-inducing-ligand). We describe some proteins regulated by p75NTR in an apoptosis condition like cytokeratin 8, 18 and 19, the HSP27 and the ribosomal protein RPLP0. These results show that the rearrangement of those proteins is associated to the survival effect of p75NTR in breast cancer cells. In a second part, we tried to identify the specific proteins partners of p75NTR for its survival pathway. For that, we applied the TAP-tag (tandem affinity purification tag) strategy, a functional proteomic approach, to the p75NTR receptor. A differential analysis by nanoLC-MS/MS mass spectrometry was conducted and we obtained a list of potentials proteins partners of the p75NTR activated survival pathway. The functional involvement of these proteins should be confirmed. Together, our work provides new data on the cellular mechanisms involved in the survival of breast cancer cells and also on the proteins partners implicated in p75NTR signaling
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Riffault, Baptiste. "Plasticité GABAergique et épilepsie : focus sur le proBDNF." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4005/document.

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Le facteur neurotrophique dérivé du cerveau (BDNF) synthétisé sous la forme d'un précurseur (proBDNF) qui peut être clivé pour donner sa forme mature (mBDNF). Le mBDNF et le proBDNF produisent des réponses physiologiques opposées par l'activation de deux classes distinctes de récepteurs transmembranaires : respectivement, le récepteur TrkB et p75NTR. Le ratio mature/pro-BDNF est un élément important impliqué dans la plasticité synaptique, la formation des circuits neuronaux et in fine les fonctions cognitives. Les altérations dans ce clivage peuvent ainsi expliquer l’émergence de conditions pathologiques post-lésionnelles, comme la mort cellulaire induite par un état de mal épileptique. Au cours de ma thèse, j'ai montré que l'altération de la maturation du BDNF in vitro, provoquait, via le récepteur p75NTR, une altération de l’activité GABAergique. Par ailleurs, au cours des crises d'épilepsies, les réponses dépolarisantes et excitatrices du GABA, soutenus par la baisse d’expression et d’activité du co-transporteur KCC2, ont été rapportées. Ainsi, in vivo, j’ai montré que la voie proBDNF/p75NTR module l'homéostasie chlore au cours du développement et dans des processus d’épileptogenèse. Pendant le développement, l’activation de la voie proBDNF/p75NTR contrôle le passage d’un GABA immature dépolarisant à un GABA mature hyperpolarisant via KCC2. Pendant l’épileptogenèse, le proBDNF via p75NTR contribuerait à l’hyperexcitabilité des réseaux neuronaux. De plus, le blocage de p75NTR permet de réduire le nombre de crises épileptiques. En conclusion, proBDNF/p75NTR est un facteur clé dans la séquence maturative du GABA et dans la mise en place de l’épilepsie du lobe temporal
The brain-derived neurotophic factor (BDNF) is synthesized as a precursor (proBDNF) that can be processed intracellularly to the mature form (mBDNF). mBDNF and proBDNF are assumed to produce opposing physiological responses mediated by the activation of two distinct classes of transmembrane receptors, the TrkB and the p75NTR respectively. The proteolysis of proBDNF is crucial for cognitive functions; its impairment may account for the emergence of brain disorders such as epilepsy. During my thesis, I showed that alteration in BDNF maturation in vitro triggers an up-regulation of p75NTR, inducing a disruption of GABAergic transmission. Moreover, in epilepsy, depolarizing and excitatory GABAergic responses, due to alteration of KCC2, have been reported. Interestingly, I described novel insights into the proBDNF/p75NTR mechanisms and function in vivo in modulating chloride homeostasis during the development of neuronal networks and in the pathogenesis of epilepsy. In physiological conditions, p75NTR activation by proBDNF may be a key regulator in shaping neural circuitry and synaptic plasticity. Moreover, I have shown that proBDNF/p75NTR to mBDNF/TrkB ratio may control the timing of the developmental shift of GABA depolarizing to hyperpolarizing. During epileptogenesis, proBDNF via p75NTR alters the excitatory/inhibitory equilibrium thereby enhancing neuronal activity through the inhibition of KCC2 function. Hence, blockade of p75NTR can prevent some of the epileptogenic mechanisms. Altogether, these data provide the first compelling evidence that proBDNF disrupts the GABA excitatory/inhibitory developmental sequence, which then favors the emergence of epileptic disorders
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Allington, Christopher. "Characterizing the interaction of NGF with p75ntr in chick retinal cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ52871.pdf.

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Okumura, Tomoyuki. "Neurotrophin receptor p75NTR characterizes human esophageal keratinocyte stem cells in vitro." Kyoto University, 2004. http://hdl.handle.net/2433/147538.

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Howell, Jenny L. "BH-3-domain-only proteins are key regulators of p75NTR-mediated apoptosis." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81343.

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The p75 neurotrophin receptor (p75NTR) is a member of the Tumor Necrosis Factor Receptor (TNFR) superfamily. Similar to TNFR members, p75NTR has been reported to mediate programmed cell death (PCD) in a variety of systems, including during development and in response to central nervous system (CNS) injury. However, in contrast to TNFR members, which typically signal via Caspase 8 to elicit cell death, studies conducted in our laboratory have demonstrated that p75NTR induces cell death via an intrinsic mitochondrial death cascade involving c-Jun N-terminal kinase (JNK) activation, mitochondrial cytochrome c release and activation of Caspases 9, 3 and 6.
In an effort to determine the mechanism by which JNK communicates with the mitochondria, we examined downstream targets of JNK including the BH3-domain-only proteins. BH3-domain-only proteins are members of the Bcl-2 family of proteins, which have been dubbed mitochondrial gate-keepers, referring to their ability to regulate release of mitochondrial proteins such as cytochrome c in response to apoptotic stimuli. Our studies revealed that p75NTR overexpression does not transcriptionally upregulate BH3-domain-only proteins, rather, it results in phosphorylation of BH3 proteins, Bad and BimEL at Serines 128 and 65, respectively, in a JNK-dependent manner. Furthermore, through loss of function studies employing RNA interference constructs targeting either Bad or Bim, as well as Bad S 128A- or BimEL S65A dominant negative constructs, we demonstrated that Bad is critical for p75NTR-mediated apoptosis, while BimEL may contribute but is less critical. Together, these studies reveal key roles for BH3-domain-only proteins in p75NTR-mediated apoptosis.
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Book chapters on the topic "P75NTR"

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Almeida, Ramiro D., and Carlos B. Duarte. "p75NTR Processing and Signaling: Functional Role." In Handbook of Neurotoxicity, 1899–923. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_25.

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Ramer, Matt S., Simon A. Bedard, and Angela L. M. Scott. "Neurotrophins and p75NTR in Axonal Regeneration and Myelination." In Handbook of Neurotoxicity, 1787–803. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_45.

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Shen, Lin-Lin, Fan Zeng, Khalil Saadipour, Jian-Jun Lu, Xin-Fu Zhou, and Yan-Jiang Wang. "p75NTR: A Molecule with Multiple Functions in Amyloid-β Metabolism and Neurotoxicity." In Handbook of Neurotoxicity, 1–17. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71519-9_28-1.

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Wang, Yan-Jiang, Fan Zeng, Khalil Saadipour, Jian-Jun Lu, and Xin-Fu Zhou. "p75NTR: A Molecule with Multiple Functions in Amyloid-Beta Metabolism and Neurotoxicity." In Handbook of Neurotoxicity, 1925–44. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_28.

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Shen, Lin-Lin, Fan Zeng, Khalil Saadipour, Jian-Jun Lu, Xin-Fu Zhou, and Yan-Jiang Wang. "p75NTR: A Molecule with Multiple Functions in Amyloid-β Metabolism and Neurotoxicity." In Handbook of Neurotoxicity, 1729–45. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15080-7_28.

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Saragovi, H. Uri, Alba Galán, and Pablo F. Barcelona. "CHAPTER 5. Modulation of p75NTR/Pro-NGF as a Therapeutic Approach for Degenerative Retinopathies." In Drug Discovery, 76–87. Cambridge: Royal Society of Chemistry, 2018. http://dx.doi.org/10.1039/9781788013666-00076.

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Okumura, Tomoyuki, Tetsuji Yamaguchi, Toru Watanabe, Takuya Nagata, and Yutaka Shimada. "Clinical Relevance of a Candidate Stem Cell Marker, p75 Neurotrophin Receptor (p75NTR) Expression in Circulating Tumor Cells." In Advances in Experimental Medicine and Biology, 247–54. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55947-6_13.

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Okumura, Tomoyuki, Tetsuji Yamaguchi, Toru Watanabe, Takuya Nagata, and Yutaka Shimada. "Flow Cytometric Detection of Circulating Tumor Cells Using a Candidate Stem Cell Marker, p75 Neurotrophin Receptor (p75NTR)." In Methods in Molecular Biology, 211–17. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7144-2_18.

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Djakiew, Daniel. "NSAID Induction of p75NTR in the Prostate: A Suppressor of Growth and Cell Migration Via the p38 MAPK Pathway." In Prostate Cancer - Original Scientific Reports and Case Studies. InTech, 2011. http://dx.doi.org/10.5772/25659.

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Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "p75NGFR." In The Gene Knockout FactsBook, 850–51. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50468-3.

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Conference papers on the topic "P75NTR"

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Chen, Wenhong, Christine N. McMahan, Keith D. Barlow, Dennis Juarez, and Linda J. Metheny-Barlow. "Abstract A64: Identification of p75NTR/TrkB-BDNF axis in breast cancer brain metastasis." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a64.

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Alshehri, Mana, Bo Young Ahn, Xiuling Wang, Shiekh Tanveer, Jennifer Chan, Donna L. Senger, and Stephen M. Robbins. "Abstract A32: Cell autonomous and cell non-autonomous roles of p75 neurotrophin receptor (p75NTR) in glioma invasion." In Abstracts: AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.brain15-a32.

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Wynne, Shehla, and Daniel Djakiew. "Abstract 1263: Induction of nonsteroidal anti-inflammatory drug-activated gene-1 (Nag-1) by NSAIDs: role of p75NTR." 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.am10-1263.

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Khwaja, Fatima, Isadora Posey, Xueqing Song, Shehla Wynne, and Daniel Djakiew. "Abstract A33: Superior efficacy of dietary 3,3’diindolylmethane (DIM) amongst several indoles to inhibit prostate cancer growth via induction of the p75NTR tumor suppressor protein." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-a33.

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Bapat, Aditi A., Ruben M. Munoz, Saaiqa Maredia, Daniel D. Von Hoff, and Haiyong Han. "Abstract B152: Modulating the activity of nerve growth factor (NGF) and its receptors tropomyosin-related kinase A (TRKA) and p75 neurotrophin receptor (p75NTR) in perineural invasion (PNI) in pancreatic cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b152.

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Yue, WeiYing, Erika Woodson, Geir Tryggvason, Jason J. Clark, and Marlan R. Hansen. "Abstract 4008: p75NTRis overexpressed in vestibular schwannomas and protects cells from apoptosis due to suppressed c-Jun N-terminal kinase (JNK) activity." 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.am10-4008.

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Reports on the topic "P75NTR"

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Wynne, Shehla. Induction of the p75NTR by Aryl Propionic Acids in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada508209.

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Quann, Emily. Induction of the p75NTR by Aryl Propionic Acids in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, December 2007. http://dx.doi.org/10.21236/ada478245.

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