Дисертації з теми "Neuronal signaling"
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Sann, Sharon Bree. "Neuronal development roles of calcium signaling /." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3259060.
Повний текст джерелаTitle from first page of PDF file (viewed June 21, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Yang, Silei. "Rapid neuronal signaling cascades initiated by corticosterone." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-148762.
Повний текст джерелаO'Hare, Michael J. "Cell cycle related signaling in neuronal death." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/29368.
Повний текст джерелаTornieri, Karine. "Signaling Mechanisms Regulating Neuronal Growth Cone Dynamics." Digital Archive @ GSU, 2008. http://digitalarchive.gsu.edu/biology_diss/48.
Повний текст джерелаRogoz, Katarzyna. "Signaling Mechanisms in the Neuronal Networks of Pain and Itch." Doctoral thesis, Uppsala universitet, Genetisk utvecklingsbiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-183255.
Повний текст джерелаCui, Rui. "The role of Ryanodine receptors in neuronal calcium signaling." Scholarly Commons, 2008. https://scholarlycommons.pacific.edu/uop_etds/705.
Повний текст джерелаGuo, Jing. "Studying the signaling pathways in ROS-induced neuronal cell death /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20GUO.
Повний текст джерелаSuen, Ka-chun, and 孫嘉俊. "Molecular signaling of neuronal apoptosis in beta-amyloid peptide neurotoxicity." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31245961.
Повний текст джерелаFigueroa-Masot, Xavier Andres. "The role of JNK signaling and Bcl-2 in neuronal function : from apoptosis to neuron excitability /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/10647.
Повний текст джерелаKrjukova, Jelena. "Investigation on Pre- and Postsynaptic Ca2+ Signaling in Neuronal Model Systems." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4300.
Повний текст джерелаTraynham, Christopher J. "Effects of Neuronal Nitric Oxide Synthase Signaling On Myocyte Contractile Function." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1305058816.
Повний текст джерелаRamos, Fresnida. "Neuronal insulin signaling and the regulation of mammalian lifespan a dissertation /." San Antonio : UTHSC, 2008. http://proquest.umi.com.libproxy.uthscsa.edu/pqdweb?did=1588771411&sid=2&Fmt=2&clientId=70986&RQT=309&VName=PQD.
Повний текст джерелаTeo, Jia-Ling. "Presenilin-1 and TCF/[beta]-catenin signaling : effects on neuronal differentiation /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/9311.
Повний текст джерелаJavier, Torrent Míriam. "Role of PS/γ-secretase-mediated signaling during neuronal development and degeneration". Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/666905.
Повний текст джерелаPresenilin-1 (PS1), the catalytic component of γ-secretase that regulates the processing of multiple transmembrane proteins is mutated in the majority of cases of familial Alzheimer’s disease (FAD). Recent evidence indicates that FAD-linked PS1 mutations reduce the γ-secretase cleavage of several transmembrane proteins, suggesting a loss-of-function mechanism. Indeed, PS1 inactivation during embryogenesis leads to morphological defects, whereas genetic inactivation of both PS in the adult brain causes age-dependent memory impairments and neurodegeneration. Moreover, the participation of PS in the proteolysis of signaling molecules involved in the development of nervous system, including ErbB4, suggest that these signaling pathways could contribute to neurodegeneration. In this doctoral thesis we have studied the role of PS1/γ-secretase-dependent cleavage of EphA3 and Nrg1/ErbB4 signaling in neuronal development and neurodegeneration. Our results show that PS1/γ-secretase is required for axon growth in the developing brain. PS1/γ-secretase mediates axon elongation through the cleavage of EphA3 at Tyr560 resulting in the generation of an ICD fragment. EphA3 ICD regulates negatively RhoA, and interacts with and increases phosphorylation (S1943) of non-muscle myosin IIA (NMIIA) leading to filament disassembly and axon growth. In contrast to the classical ephrin/EphA3 signaling, PS/γ-secretase-dependent EphA3 signaling is independent of ligand. This result suggests for the first time opposite roles of EphA3 on inhibiting (ligand-dependent) and enhancing (PS/γ-secretase-dependent processing) axon growth in neurons. Second, we show that PS/γ-secretase regulates Nrg1 type III expression, mediates the processing of Nrg1 type III and ErbB4 and regulates negatively synaptogenesis through Nrg1. Taken together, our results show that PS1/γ-secretase regulates axon growth and synaptogenesis by regulating ligand-independent EphA3 signalling and Nrg1/ErbB4 processing/signalling, respectively. Our investigation paves the way for exploring new relationships between neurodevelopment and neurodegeneration, providing insights of the existence of a crosstalk among the signaling pathways involved in these processes.
Roux, Philippe P. "Signaling pathways implicated in p75 neurotrophin receptor-mediated neuronal survival and death." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38267.
Повний текст джерелаNervous system injuries represent interesting models to study p75NTR because several types of injury induce p75NTR expression. In the first part of this thesis, we have used the pilocarpine model of seizure in the rat and found that this type of injury induces neuronal apoptosis and p75NTR expression. Apoptosis was tightly linked with p75NTR expression, suggesting that p75NTR may promote apoptosic cell death after seizure, and consistent with this, we have found that p75NTR can promote JNK activation and apoptosis in vitro. In the second study, we discovered that p75NTR can also facilitate survival under some cellular circumstances. The survival-promoting effect of p75NTR was accompanied with PI3-K-dependent Akt activation, and correlated with a reduction in cytosolic protein tyrosine phosphatase activity, suggesting that p75NTR may regulate a tyrosine phosphatase involved in the regulation of Akt and survival. In the last study, we have found that the related neuroprotective compounds, K252a and CEP 1347, are potent. MLK3 inhibitors, yet they simultaneously activated Akt and ERK, and survival through MLK3-independent mechanisms. These findings suggested that K252a and CEP1347 may act on a novel target responsible for their survival-promoting activities.
Taken together, the data in this thesis adds to our understanding of the physiological functions of p75NTR, and contributes to our knowledge of the cellular machinery that control neuronal cell survival and death.
Yang, Silei [Verfasser], and Rainer [Akademischer Betreuer] Landgraf. "Rapid neuronal signaling cascades initiated by corticosterone / Silei Yang. Betreuer: Rainer Landgraf." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1027066143/34.
Повний текст джерелаWang, Xinnan. "Neuronal and signaling roles of a Drosophila hereditary spastic paraplegia gene SPG6." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612846.
Повний текст джерелаShoop, Richard D. "Localization and calcium signaling of neuronal nicotinic acetylcholine receptors on somatic spines /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9975047.
Повний текст джерелаMuta, Kenjiro. "The role of neuronal mTORC1 signaling in the regulation of physiological processes." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/1706.
Повний текст джерелаJiang, Xiaosong. "Muscle induces neuronal expression of acetylcholinesterase in neuron-muscle co-culture : transcription regulation mediated by cAMP-dependent signaling /." View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202003%20JIANG.
Повний текст джерелаIncludes bibliographical references (leaves 132-149). Also available in electronic version. Access restricted to campus users.
Kam, Ka-man. "Expression analysis of Hoxb5 in enteric neurons and generation of Tamoxifen inducible Cre mice for neuronal Hoxb5 signaling perturbation." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290574.
Повний текст джерелаMiloş, Ruxandra-Iulia. "In vivo analysis of the neuronal calcium signaling in the developing visual cortex." kostenfrei, 2008. http://mediatum2.ub.tum.de/doc/627379/627379.pdf.
Повний текст джерелаRoof, Steve. "Neuronal Nitric Oxide Synthase Signaling Contributes to the Beneficial Cardiac Effects of Exercise." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354048916.
Повний текст джерелаJohnson, Christopher M. "Investigating the Slow Axonal Transport of Neurofilaments: A Precursor for Optimal Neuronal Signaling." Ohio University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1452018547.
Повний текст джерелаNg, Yu Pong. "Leukemia inhibitory factor receptor signaling in NGF-induced neuronal differentiation of PC12 cells /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BICH%202004%20NG.
Повний текст джерелаIncludes bibliographical references (leaves 134-172). Also available in electronic version. Access restricted to campus users.
Mejia, Luis Antonio. "Interaction Proteomics of Autism Spectrum Disorder- and Intellectual Disability-Associated Proteins Identifies a Novel Hap1-Tsc1 Signaling Link that Controls Neuronal mTORC1 Signaling and Pyramidal Neuron Morphogenesis." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11190.
Повний текст джерелаArthur, David Benjamin. "Extracellular nucleotide signaling in neuronal differentiation and survival Multiple roles of the P2Y₂ receptor /." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3205808.
Повний текст джерелаTitle from first page of PDF file (viewed April 3, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 139-159).
Coffill, Cynthia Rose. "The study of signaling pathways controlling neuronal apoptosis inhibitory protein (NAIP) expression and function." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/29345.
Повний текст джерелаKrjukova, Jelena. "Investigation on Pre- and Postsynaptic Ca2+ Signaling in Neuronal Model Systems." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4300.
Повний текст джерелаGarcia, Rodrigo I. S. M. Massachusetts Institute of Technology. "Cell-type specific contributions to Rett Syndrome : neuronal and astrocytic signaling and sensory processing." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/106431.
Повний текст джерелаPage 127 blank. Cataloged from PDF version of thesis.
Includes bibliographical references.
Loss of function mutations in the X-linked gene encoding for MeCP2 are the underlying genetic cause for Rett Syndrome (RTT), a devastating neurodevelopmental disorder that primarily affects girls. While the function of this transcriptional regulator remains elusive and complex, recent focus has turned to downstream signaling pathways as putative targets for novel therapeutics. The complexity of MeCP2 function is compounded by the heterogeneity of cell types in the brain, with recent evidence implicating glia cells in RTT pathophysiology. The focus of my thesis has been two-fold: exploring signaling mechanisms downstream of MeCP2 and the potential of IGF-1 as a therapeutic for RTT, and examining functional astrocyte sensory processing in healthy and impaired circuits. I present evidence that IGF-1 levels are reduced in mouse models of RTT and systemic treatment with IGF-1 leads to improvements in lifespan, respiratory patterns, and social behaviors. These effects are accompanied by increased synaptic proteins, activation of signaling pathways, and enhanced excitatory transmission, as well as effects on plasticity in visual cortex circuits. Astrocytes, known to contribute to synapse formation and maintenance, have been implicated alongside neurons as contributors to the RTT phenotype. They express the two most abundant glutamate transporters in the brain responsible for the majority of glutamate clearance from synapses. Indeed, lack of MeCP2 in astrocytes leads to a reduction in signaling pathways and aberrant glutamate transporter expression, with strong implications for synaptic and circuit activity. Efficient processing of visual information requires processing salient features while overcoming the inherent variability in neuronal networks. Natural movies evoke reliable responses from pyramidal neurons in visual cortex and my work reveals that discrete microdomain regions of visual cortex astrocytes also exhibit temporally reliable and spatially correlated responses to natural scenes. I show that glutamate transporters, which influence astrocytic Ca 2 signaling and synaptic transmission, regulate the reliability of astrocyte microdomain responses and thus contribute crucially to visual information processing. Finally, I show that in a RTT mouse model, astrocyte microdomains elicited by visual stimuli are reduced in size, consistent with the reduced synaptic transmission and neuronal responses observed in these mice.
by Rodrigo I. Garcia.
Ph. D. in Neuroscience
Tang, Lifei. "Effects of Neuronal Nitric Oxide Synthase Signaling on Myocyte Contraction during Beta-Adrenergic Stimulation." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1385336408.
Повний текст джерелаStepan, Jens [Verfasser], and Angelika [Akademischer Betreuer] Erhardt. "Enhanced endocannabinoid signaling modulates neuronal network dynamics in the hippocampus / Jens Stepan ; Betreuer: Angelika Erhardt." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1160875855/34.
Повний текст джерелаMoore-Dotson, Johnnie M., Jamie J. Beckman, Reece E. Mazade, Mrinalini Hoon, Adam S. Bernstein, Melissa J. Romero-Aleshire, Heddwen L. Brooks, and Erika D. Eggers. "Early Retinal Neuronal Dysfunction in Diabetic Mice: Reduced Light-Evoked Inhibition Increases Rod Pathway Signaling." Association for Research in Vision and Ophthalmology (ARVO), 2016. http://hdl.handle.net/10150/604678.
Повний текст джерелаKaur, Shilpa. "Role of Wnt signaling in the polarization of neuronal precursors in the C. elegans embryo." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0068.
Повний текст джерелаIn both vertebrates and invertebrates neurons are often produced by asymmetric cell divisions. Some components of the Wnt pathway have been implicated in this process. However, how Wnt ligands, secreted activators of the Wnt pathway, regulate these divisions is not understood. The aim of my PhD is to analyze the role of Wnt ligands and of their receptors in neuronal precursor asymmetric divisions using C. elegans as a model organism. In the C. elegans embryo, neuronal precursors divide asymmetrically along the antero-posterior axis. The host laboratory has shown that these asymmetric divisions are regulated by a nuclear component of the Wnt pathway, beta-catenin, which accumulates specifically in the nucleus of the posterior daughter cell following asymmetric cell division. During my PhD, I analyzed the role of extracellular and cortical components in the asymmetric divisions of neuronal precursors using the AIY cholinergic lineage as a test lineage. I first observed that neuronal precursors are elongated along the antero-posterior axis before their division. Three Wnt ligands (CWN-1, CWN-2 and MOM-2) are transcribed at a higher level in the posterior region of the embryo. Using loss and gain of function experiments, I have observed that the Wnt ligands regulate the orientation of the divisions as well as the asymmetry in the identity of the daughter cells. I also identified a role for the Wnt receptor MOM-5 and the cortical protein APC during these asymmetric divisions. MOM-5 is enriched at the posterior pole and APC at the anterior pole of the neuronal precursors before their divisions
Han, Jing. "ROLE OF THE REGULATOR OF G PROTEIN SIGNALING 2 (RGS2) FOR NEURONAL AND SYSTEM FUNCTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1175703706.
Повний текст джерелаBrusich, Douglas J. "Dual roles for an intracellular calcium-signaling pathway in regulating synaptic homeostasis and neuronal excitability." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1830.
Повний текст джерелаLogin, Hande. "Activity-regulated retinoic acid signaling in olfactory sensory neurons." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-89022.
Повний текст джерелаFleegal, Melissa A. "Angiotensin II modulation of neuronal intracellular signaling cascades regulates short-term and long-term physiological responses." [Gainesville, Fla.] : University of Florida, 2002. http://purl.fcla.edu/fcla/etd/UFE1001140.
Повний текст джерелаKoemeter-Cox, Andrew I. "The Role of the Neuronal Primary Cilium in the Modulation of G Protein-Coupled Receptor Signaling." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1408891463.
Повний текст джерелаHashmi, Fiza. "EFFECTS OF BRAIN-DERIVED NEUROTROPHIC FACTOR AND ITS SIGNALING PATHWAY ON SENSORY NEURONAL ACTIVATION DURING COLITIS." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3980.
Повний текст джерелаDian, Emese Emöke. "Application of Cultured Neuronal Networks for Use as Biological Sensors in Water Toxicology and Lipid Signaling." Thesis, University of North Texas, 2004. https://digital.library.unt.edu/ark:/67531/metadc5557/.
Повний текст джерелаTraub, Stefanie Andrea [Verfasser]. "Establishment of a human iPS cell-derived neuronal model cell to study synaptic signaling / Stefanie Andrea Traub." Konstanz : KOPS Universität Konstanz, 2020. http://d-nb.info/1206538910/34.
Повний текст джерелаDixon, Salazar Tracy Jean. "Major histocompatibility complex class I is a negative regulator of neuronal insulin receptor signaling and hippocampal synapse number." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3386747.
Повний текст джерелаTitle from first page of PDF file (viewed Jan. 19, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 65-71).
Frazier, Hilaree N. "Exploring the Role of Insulin Receptor Signaling in Hippocampal Learning and Memory, Neuronal Calcium Dysregulation, and Glucose Metabolism." UKnowledge, 2019. https://uknowledge.uky.edu/pharmacol_etds/32.
Повний текст джерелаSandberg, Malin. "Calcium dynamics and vesicle-release proteins in a prion-infected neuronal cell line /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-245-4/.
Повний текст джерелаKarolewicz, Beata, Laurel Johnson, Katalin Szebeni, Craig A. Stockmeier, and Gregory A. Ordway. "Glutamate Signaling Proteins and Tyrosine Hydroxylase in the Locus Coeruleus of Alcoholics." Digital Commons @ East Tennessee State University, 2008. https://dc.etsu.edu/etsu-works/8610.
Повний текст джерелаLadarré, Delphine. "Neuronal polarization shapes the targeting and signaling of G-protein coupled receptors (GPCRs) : type-1 cannabinoid receptors and 5-HT1B serotonin receptors show highly contrasted trafficking and signaling patterns in axons and dendrites." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T070/document.
Повний текст джерелаPolarized neuronal architecture is achieved and maintained mainly through highly controlled targeting of proteins to axons versus to the somatodendritic compartment. Among these proteins, neuronal G protein coupled receptors (GPCRs) are key therapeutic targets. However, their pharmacology is generally studied in non-polarized cell lines, and results obtained in such systems likely do not fully characterize the physiological effects of brain GPCR activation. Therefore, a main research subject of our group is to understand how neuronal polarity influences GPCR pharmacology, by studying one of the most abundant GPCR in the brain: the type-1 cannabinoid receptor (CB1R). Previous studies of the group suggested that CB1Rs achieve axonal polarization through transcytotic targeting: after their synthesis, these receptors appear on the somatodendritic plasma membrane from where they are removed rapidly by constitutive endocytosis and then targeted to the axonal plasma membrane where they accumulate due to relatively reduced endocytosis rate. At the beginning of my PhD project we directly demonstrated this differential endocytosis and transcytotic transport of CB1Rs by using cultured neurons in microfluidic devices. Moreover, we showed that chronic pharmacological treatments may strongly change neuronal GPCR distribution on the neuronal surface. These results demonstrate that subdomain-dependent steady-state endocytosis, which is pharmacologically controllable, is important for GPCR distribution in neurons. In a second part, we asked if differential traffic of CB1Rs between axons and dendrites is correlated with differential pharmacology. CB1R is predominantly coupled to Gi/o proteins and is known to inhibit cAMP production. Thus, we developed live Föster Resonance Energy Transfer (FRET) imaging in cultured hippocampal neurons in order to measure basal cAMP/PKA pathway modulation downstream of endogenous CB1Rs in all neuronal compartments: in somata, in dendrites but also in the very thin mature axons. Our results show that CB1R displays differential pharmacology between axon and dendrites. Notably, its activation leads to a stronger decrease of PKA activity in axons compared to dendrites, due to increased number of membrane receptors in this compartment. Moreover, we demonstrate that somatodendritic CB1Rs constitutively inhibit cAMP/PKA pathway, while axonal receptors do not. This difference is due to polarized distribution of DAGLipase, the enzyme that synthesizes the major endocannabinoid 2-arachidonoylglycerol (2-AG). Moreover, blocking DAGL by pharmacological treatment modifies somatodendritic, but not axonal effects of several CB1R agonists, possibly through allosteric action. In a third part, we asked if the above results may be generalized to other GPCRs. Because the axonal targeting and in vitro pharmacology of 5-HT1B serotonin receptors demonstrate strong similarities with CB1Rs, we studied their neuronal pharmacology by using the previously developed FRET technique. We found similar differential responses to pharmacological treatments between axon and dendrites. In a fourth part, we investigated the role of the threonine 210 (T210) residue in the constitutive activity of neuronal CB1R. We showed that the hypoactive mutant T210A-CB1R do not constitutively recruit signaling pathways even in somatodendritic compartment, where 2-AG is present. This result demonstrates that T210 is necessary for constitutive CB1R activation by 2-AG.Finally, previous results of our group demonstrated the involvement of CB1R in neuronal development. Notably, CB1R activation was shown to have an overall inhibitory effect on the development of polarized neuronal morphology. We established a bibliographic review on this subject. The published literature data suggest that not only neuronal polarization influences both CB1R traffic and pharmacology but CB1Rs also contribute to the achievement of neuronal polarization. (...)
Brumback, Audrey Christine. "Thermodynamic regulation of NKCC1-mediated chloride transport underlies plasticity of GABAA signaling /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 86-96). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Alp, Murat. "A kinetic model of calcium binding to calretinin : experimental measurements and predicted effects on calcium signaling at neuronal synapses /." view abstract or download file of text, 2005. http://wwwlib.umi.com/cr/uoregon/fullcit?p3190505.
Повний текст джерелаTypescript. Includes vita and abstract. Includes bibliographical references (leaves 250 - 269). Also available for download via the World Wide Web; free to University of Oregon users.
Bhardwaj, Deepshikha. "Phosphorylated Tyr142 β-Catenin signaling in axon morphogenesis and centrosomal functions". Doctoral thesis, Universitat de Lleida, 2014. http://hdl.handle.net/10803/285932.
Повний текст джерелаβ-catenina es una proteína multifuncional, componente clave de las uniones adherentes y efector de la vía canónica Wnt, recientemente implicada en funciones centrosomales. En la señalización por Wnt, cuando Wnt está presente, β-catenina se acumula en el citosol y transloca al núcleo donde, junto con factores TCF, regula la transcripción de genes diana. La interelación entre funciones adhesivas y señalizadoras (independientes de Wnt) de β-catenina se logra, en parte, a través de la fosforilación de β-catenina en Tyr142, que promueve la desunión de β-catenina del complejo de adhesión y la migración a través de la regulación transcripcional. El receptor tirosina quinasa Met (receptor del Factor de Crecimiento Hepático (HGF)) induce la fosforilación de β-catenina en Tyr142 durante la migración y el crecimiento axonal estimulados por HGF. Por otra parte, la fosforilación de β-catenina en Ser/Thr regula la degradación de β-catenina y afecta a la cohesión/separación de los centrosomas y la formación del huso mitótico. Aquí nos centramos en la señalización por β-catenina fosforilada en Tyr142. En primer lugar, demostramos que quimiocinas de las familias CC y CXC promueven el crecimiento axonal y que las quimiocinas actúan en la señalización inducida por HGF/Met/β-catenina/TCF durante la morfogénesis del axón. También mostramos que CXCL2 promueve la ramificación del axón en neuronas hipocampales y el crecimiento de axones sensoriales de los ganglios de la raíz dorsal. En segundo lugar, demostramos que β-catenina fosforilada en Tyr142 localiza en centrosomas en astrocitos primarios y células de glioma, y que estos niveles centrosomales disminuyen durante la mitosis. También mostramos la localización centrosomal de Met activo. Con objeto de identificar cual es la quinasa que regula la fosforilación de Tyr142 β-catenina en el centrosoma, mostramos que un inhibidor de Syk disminuye los niveles centrosomales de esta forma de β-catenina, lo que sugiere que Syk fosforila β-catenina en Tyr142 en el centrosoma. Además, β-catenina está implicada en el posicionamiento del centrosoma durante la migración de astrocitos y la fosforilación de β-catenina en Tyr142 es necesaria en la migración celular estimulada por HGF. En conjunto, este trabajo ilustra las múltiples funciones señalizadoras de β-catenina fosforilada en Tyr142 en la morfogénesis del axón (a través de la expresión de quimiocinas), así como en funciones centrosomales y en polaridad celular y migración.
β-catenina és una proteïna multifuncional, component clau de les unions adherents i efector de la via canònica Wnt, recentment implicada en funcions centrosomals. En la senyalització per Wnt, quan Wnt està present β-catenina s'acumula en el citosol i transloca al nucli on, juntament amb factors TCF, regula la transcripció de gens diana. La interrelació entre funcions adhesives i funcions senyalitzadores (independents de Wnt) de β-catenina s'aconsegueix en part a través de la fosforilació de β-catenina en Tyr142, que promou la desunió de β-catenina del complex d'adhesió i la migració mitjançant la regulació transcripcional. El receptor tirosina quinasa Met (receptor del Factor de Creixement Hepàtic (HGF)) regula la fosforilació de β-catenina en Tyr142 durant la migració cel · lular i el creixement axonal estimulat per HGF. D'altra banda, la fosforilació de β-catenina en Ser/Thr regula la degradació de β-catenina i afecta la cohesió/separació centrosomal i la formació del fus mitòtic. Aquí ens centrem en la senyalització per β-catenina fosforilada en Tyr142. En primer lloc, demostrem que quimiocines de les famílies CC i CXC promouen el creixement axonal i que la senyalització per quimiocines és necessària en la senyalització induïda per HGF/Met/β-catenina/TCF durant la morfogènesi axonal en neurones de l'hipocamp. També mostrem que CXCL2 promou la ramificació de l'axó i que aquesta quimiocina està involucrada en el creixement d'axons sensorials dels ganglis de l'arrel dorsal. A la segona part, demostrem que β-catenina fosforilada en Tyr142 es localitza en els centrosomes en astròcits primaris i cèl · lules de glioma, i que els seus nivells centrosomals disminueixen durant la mitosi. A més, demostrem la localització centrosomal de Met actiu. Amb l'objectiu d'identificar quina és la quinasa que regula els nivells centrosomals de fosfo-Tyr142 β-catenina, mostrem que un inhibidor de Syk disminueix els nivells centrosomals de fosfo-Tyr142 β-catenina, el que suggereix que Syk fosforila β-catenina en Tyr142 al centrosoma. A més, β-catenina està implicada en el posicionament del centrosoma durant la migració d'astròcits i la fosforilació de β-catenina en Tyr142 és necessària en la migració cel.lular estimulada per HGF. En conjunt, aquest treball demostra les múltiples funcions senyalitzadores de β-catenina fosforilada en Tyr142, en la morfogènesi de l'axó (a través de la regulació de l'expressió de quimiocines), així com en funcions centrosomals i en polaritat cellular i migració.