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Dissertations / Theses on the topic 'FMR1 protein'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Hall, Deborah A. "Prevalence of FMR1 repeat expansions in movement disorders /." Connect to abstract via ProQuest. Full text is not available online, 2008. http://proquest.umi.com/pqdweb?did=1545571851&sid=1&Fmt=6&clientId=18952&RQT=309&VName=PQD.

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Thesis (Ph.D. in Clinical Science) -- University of Colorado Denver, 2008.<br>Typescript. Includes bibliographical references (leaves 59-67). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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2

Verheij, Coleta. "Characterization of the FMR1 protein involved in the fragile X syndrome." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 1996. http://hdl.handle.net/1765/13734.

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3

Banerjee, Paromita. "Modeling the Effects of FMR1 Alleles on Behavioral and Synaptic Plasticity." Miami University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=miami1217359939.

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4

Velloso, Fernando Janczur. "Variabilidade do domínio KH-2 da proteína do retardo mental do X frágil (FMRP)." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-21032014-090729/.

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A proteína do retardo mental do X frágil (FMRP), codificada pelo gene do Retardo Mental do X Frágil (do inglês, Fragile Mental Retardation 1, FMR1) tem expressão significativa no encéfalo, gônadas e células proliferativas. A FMRP é uma proteína ligante de RNA, repressora traducional, que transita entre o núcleo celular, grânulos citoplasmáticos e polissomos. Sua associação a RNA pode se dar pelos domínios Tudor N-terminais, dois domínios centrais, com homologia à heteronucleoproteína K (KH) ou motivos RGG, ricos em arginina (R) e glicina (G), C-terminais. A abolição da expressão da FMRP por mu

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5

ZALFA, FRANCESCA. "A new mechanism for regulating mRNA translation in the mammalian CNS:." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2006. http://hdl.handle.net/2108/245.

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Abstract tesi PhD Dr. Zalfa Francesca A new mechanism for regulating mRNA translation in the mammalian CNS: a role for the Fragile X Mental Retardation Protein FMRP (Fragile X Mental Retardation Protein) è una proteina che lega gli RNA altamente espressa nel cervello. L’assenza o la mutazione di FMRP causa la sindrome dell’X fragile, una disfunzione dominante legata al cromosoma X e la più frequente causa di ritardo mentale ereditario (con un’incidenza di 1 su 4000 maschi e di 1 su 6000 femmine). Utilizzando il modello murino della sindrome dell’X Fragile (il topo FMR1 knock-out), h

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6

Khayachi, Anouar. "Rôles fonctionnels de la SUMOylation de FMRP « Fragile X Mental Retardation Protein »." Thesis, Nice, 2015. http://www.theses.fr/2015NICE4031.

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Le syndrome de l’X-fragile est la forme la plus fréquente de déficience intellectuelle héréditaire liée au chromosome X. Cette maladie résulte de la mutation du gène FMR1 localisé sur le chromosome X. La protéine correspondante, FMRP, est absente chez les patients atteints de la maladie. Il faut noter ici qu’il existe un modèle murin mimant la pathologie humaine. Ainsi dans ces animaux qui n’expriment pas la protéine FMRP, les neurones présentent des anomalies architecturales de la synapse entraînant d’importants dysfonctionnements dans la transmission et la plasticité synaptique qui sont à l’

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7

NAPOLI, ILARIA. "How the fragile X mental retardation protein represses protein synthesis: a mechanism of translational control in dendrites." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/765.

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La Sindrome dell'X Fragile è la forma di ritardo mentale ereditario più frequente nella popolazione con un'incidenza 1/4000 nei maschi e 1/6000 nelle femmine. La patologia è causata da mutazioni nel gene FMR1 il cui prodotto proteico, FMRP, è altamente espresso nei neuroni. FMRP è una proteina che lega gli RNA messaggeri neuronali e si localizza lungo i dendriti e gli assoni dei neuroni dove controlla il trasporto e la sintesi proteica dei messaggeri associati. Nel presente progetto abbiamo analizzato il meccanismo attraverso il quale FMRP regola la sintesi proteica alle sinapsi, caratteri

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8

Khayachi, Anouar. "Rôles fonctionnels de la SUMOylation de FMRP « Fragile X Mental Retardation Protein »." Electronic Thesis or Diss., Nice, 2015. http://www.theses.fr/2015NICE4031.

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Le syndrome de l’X-fragile est la forme la plus fréquente de déficience intellectuelle héréditaire liée au chromosome X. Cette maladie résulte de la mutation du gène FMR1 localisé sur le chromosome X. La protéine correspondante, FMRP, est absente chez les patients atteints de la maladie. Il faut noter ici qu’il existe un modèle murin mimant la pathologie humaine. Ainsi dans ces animaux qui n’expriment pas la protéine FMRP, les neurones présentent des anomalies architecturales de la synapse entraînant d’importants dysfonctionnements dans la transmission et la plasticité synaptique qui sont à l’

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9

Wu, Yuhong. "Structural studies of Human Caprin Protein." OpenSIUC, 2019. https://opensiuc.lib.siu.edu/dissertations/1652.

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Human Caprin-1 and Caprin-2 are prototypic members of the caprin (cytoplasmic activation/proliferation-associated protein) protein family. Vertebrate caprin proteins contain two highly conserved homologous regions (HR1 and HR2) and C-terminal RGG motifs. Drosophila caprin (dCaprin) shares HR1 and RGG motifs but lacks HR2. Caprin-1 and Caprin-2 have important and non-redundant functions. The detailed molecular mechanisms of their actions remain largely unknown.

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10

Stöcker, Stefanie [Verfasser]. "Function of the Cytoplasmic FMRP Interacting Protein 1 (CyFIP1) in mouse / Stefanie Stöcker." Bonn : Universitäts- und Landesbibliothek Bonn, 2016. http://d-nb.info/1132711193/34.

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11

Wijetunge, Lasani Sulochana. "Role of mGluR5 and FMRP in mouse primary somatosensory cortex." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3886.

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The accurate development of the wiring between the billions of neurons in our brain is fundamental to brain function. Development of this connectivity relies on activity-dependent modification of synapses similar to those that underlie learning and memory. Glutamate is the principal excitatory neurotransmitter in the mammalian brain and several brain disorders result from altered glutamatergic receptor signalling (Catania et al., 2007; Lau and Zukin, 2007). Genes encoding glutamate receptor associated proteins have a high incidence of mutation in cognitive disorders, especially X-linked mental

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12

Komissarov, Artem 1992. "Reconstitution of FMRP-mediated mRNA transport system in vitro." Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/670058.

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Learning and memory formation are based on the mechanisms of synaptic plasticity. Synaptic plasticity modulates development and strengthening of new neuronal connections, or synapses, upon learning and is based on local protein synthesis next to activated neuronal spines. Thousands of mRNA species are transported from the soma of neuron to dendrites, in order to be translated on demand. The mechanisms of this mRNA transport remain poorly understood. Mutations of Fragile X-mental retardation protein (FMRP) cause a spectrum of mental retardation disorders. Among other functions, FMRP mediates

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13

Bhattacharjee, Sonali. "The role of Fml1 and its partner proteins Mhf1 and Mhf2 in promoting genome stability." Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711640.

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14

Daroles, Laura. "Le rôle de la Fragile X Mental Retardation Protein et de alpha CamKII dans la plasticité des cellules granulaires du bulbe olfactif en réponse à l'apprentissage." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066037/document.

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La Fragile X Mental Retardation Protein (FMRP) est une protéine régulant la traduction locale de nombreux ARNm dans le cerveau. Elle est absente dans le Syndrome de l'X Fragile (SXF), première cause de retard mental héréditaire. J'ai étudié le rôle de FMRP dans la plasticité structurelle des cellules granulaires (CG) produites à l'âge adulte dans le bulbe olfactif (BO) en réponse à un apprentissage chez la souris. L'apprentissage perceptif (AP) induit de profonds changements structurels des nouveaux neurones du BO adulte. En absence de FMRP dans les CG nouvellement générées, l'apprentissage et

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15

Zhuang, Yuan [Verfasser]. "Hepato-protective role of Fragile X Mental Retardation Protein (FMRP) and Immune Cells in Liver Diseases / Yuan Zhuang." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1205154906/34.

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16

Nolze, Alexander [Verfasser], Mechthild [Akademischer Betreuer] Hatzfeld, Elmar [Akademischer Betreuer] Wahle, and Michael [Akademischer Betreuer] Kiebler. "FMRP reguliert die Aktinzytoskelett-Reorganisation durch das Armadillo-Protein p0071 / Alexander Nolze. Betreuer: Mechthild Hatzfeld ; Elmar Wahle ; Michael Kiebler." Halle, Saale : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2014. http://d-nb.info/1047796406/34.

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17

Prunnbauer, Maren [Verfasser], and Stefan [Akademischer Betreuer] Kindler. "Das Fragile X Syndrom: Untersuchung neuer Interaktionspartner des RNA-bindenden Proteins FMRP / Maren Prunnbauer. Betreuer: Stefan Kindler." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://d-nb.info/102394720X/34.

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18

Petrenz, Nickolas Mirko [Verfasser]. "Das Fragile-X-Syndrom : vergleichende Analyse der zellulären Proteininteraktionsmuster der physiologischen und einer pathogenen Form des Proteins FMRP / Nickolas Mirko Petrenz." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1010759590/34.

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19

Steffens, Katharina [Verfasser], and Hans-Jürgen [Akademischer Betreuer] Kreienkamp. "Der Einfluss von FMRP (fragile x mental retardation protein) auf die Zusammensetzung dendritisch lokalisierter Ribonukleoprotein Partikel in der Maus (Mus musculus) / Katharina Steffens. Betreuer: Hans-Jürgen Kreienkamp." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2014. http://d-nb.info/105504020X/34.

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20

Tabet, Ricardos. "Bases moléculaires de la physiopathologie du syndrome de l'X fragile." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ090.

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Le syndrome de l’X fragile représente la première cause de déficience intellectuelle héréditaire. Ce syndrome résulte de l’absence de la protéine FMRP. FMRP est proposée réguler, sous contrôles des mGluR-I et d’autres récepteurs, l’expression de protéines importantes pour la plasticité synaptique en se fixant spécifiquement sur leur ARNm et en modulant leur traduction. Des milliers d’ARNm cibles ont déjà été proposées dans la littérature, mais très peu ont pu être validées. Par approche de pontage covalent aux UV et immunoprecipitation (CLIP) couplé à une analyse microarray, nous avons identif

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21

Kieffer, Félicie. "Étude par analyses protéomiques du rôle de SUMO et de FMRP dans la régulation de la diversité protéique de la synapse." Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://theses.univ-cotedazur.fr/2022COAZ6016.

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Les synapses sont des structures hautement spécialisées qui interconnectent les neurones pour former des réseaux fonctionnels dédiés à la communication neuronale. Les synapses subissent de nombreux réarrangements avec notamment des modifications constantes de leur composition protéique. Afin de créer de la diversité protéique, plusieurs processus entrent en jeu, de la transcription à la traduction locale. En effet, à partir d'un même gène, plusieurs protéines peuvent être synthétisées sous l'action de différentes étapes de maturation des ARNm. Par ailleurs, les protéines peuvent également, une

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22

Adusei, Daniel C. "Early Developmental Alterations in GABAergic Protein Expression in Fragile X Knockout Mice." Thesis, 2010. http://hdl.handle.net/1807/25402.

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The purpose of this study was to examine the expression of GABAergic proteins in Fmr1 knockout mice during brain maturation and to assess behavioural changes potentially linked to perturbations in the GABAergic system. Quantitative western blotting of the forebrain revealed that compared to wild-type mice, the GABAA receptor α1, β2, and δ subunits, and the GABA catabolic enzymes GABA transaminase and SSADH were down-regulated during postnatal development, while GAD65 was up-regulated in the adult knockout mouse forebrain. In tests of locomotor activity, the suppressive effect on motor activi

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23

Tabatabaei, Dina. "Expression of interleukin-6 (IL-6) in the cerebellum is not altered in the absence of Fragile X Mental Retardation Protein (FMRP) or with motor skill learning." 2016. http://hdl.handle.net/1993/31638.

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The ability of the brain to change structurally and functionally with experience is called brain plasticity. High levels of pro-inflammatory cytokines impair normal memory formation and consolidation. To better understand the role of pro-inflammatory cytokines in learning, the contribution of the cytokine interleukin-6 (IL-6) to a motor skill learning task investigated. The Fmr1 Knockout (KO) mouse, an animal model of Fragile X Syndrome, has demonstrated impaired neural plasticity and learning. Fmr1 KO and control wild-type (WT) mice were trained on the dowel and flat beam runways to study mo

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24

Majaess, Namat-Maria. "A Loss of the Fragile X mental retardation protein alters the spatial and temporal expression of glutamate receptors in the mouse brain." Thesis, 2012. http://hdl.handle.net/1828/4372.

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Fragile X Syndrome (FXS) is the leading cause of inherited intellectual disability. The disorder is caused by a trinucleotide expansion that silences the Fragile X Mental Retardation 1 (Fmr1) gene resulting in the loss of its protein product, the Fragile X Mental Retardation Protein (FMRP). FXS patients show broad clinical phenotypes including intellectual disability, as well as a number of cognitive and behavioral problems. The lack of FMRP is believed to be the direct cause of the deficits seen in FXS patients. FMRP is an RNA-binding protein that is expressed in the brain and testes. This p

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25

Shang, Yuze. "Fragile X Mental Retardation Protein is Required for Chemically-induced Long-term Potentiation of the Hippocampus in Adult Mice." Thesis, 2009. http://hdl.handle.net/1807/18857.

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Fragile X syndrome (FXS) is caused by the lack of fragile X mental retardation protein (FMRP). The animal model of FXS, Fmr1 knockout (KO) mice, shows impairment in hippocampus-dependent learning and memory. However, results for long-term potentiation (LTP), remain inconclusive in the hippocampus of Fmr1 KO mice. Here, we demonstrate that FMRP is required for glycine-induced LTP (Gly-LTP) in the CA1 of hippocampus. The Gly-LTP requires activation of postsynaptic NMDA receptors and metabotropic glutamateric receptors, as well as the subsequent activation of extracellular signal-regulated ki

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