Dissertations / Theses on the topic 'Arrestin Proteins'
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Celver, Jeremy Phillip. "Molecular mechanisms of opioid receptor regulation by GRK and arrestin /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/6299.
Full textWilham, Laura Elizabeth. "The role of [beta]-arrestin in agonist-induced down-regulation of the M₁mAChR." CONNECT TO THIS TITLE ONLINE, 2006. http://etd.lib.umt.edu/theses/available/etd-03022007-104437/.
Full textParisis, Nikolaos. "Identification of PAR-2-regulated ERK substrates and (Beta)-arrestin-interacting proteins in invasive breast cancer cells." Thesis, University of Essex, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520107.
Full textBengreed, Amal H. I. "Characterisation of P2Y receptor-mediated contractile signalling and its regulation by G protein coupled receptor kinases and arrestin proteins in a rat bladder smooth muscle." Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/42795.
Full textDavidson, Reshma. "Regulation of Septum Formation by Two Novel Proteins Art1 and Bga1 in Fission Yeast Cytokinesis." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1469185292.
Full textFessart, Delphine. "Regulation of the endocytic adaptor proteins [beta] arrestin and AP-2 during clathrin-mediated internalization of Angiotensin II type 1 receptor." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102501.
Full textThe internalization of Angiotensin II (Ang II) type 1 receptor (AT1R) is controversial and poorly described. Therefore, our laboratory studies the mechanisms behind AT1R internalization. The agonist-induced internalization of AT1R begins with the formation of a complex including betaarrestin, the clathrin adaptor AP-2, and the tyrosine protein kinase, c-Src. In turn, this c-Src recruitment regulates the clathrin-mediated internalization of AT1R by controlling the formation of endocytic complexes during endocytosis. Indeed, the recruitment of c-Src is involved in the dissociation of AP-2 during receptor internalization. Based on our evidence that AP-2 and c-Src can be found in the same complex, we suggested that AP-2 could be phosphorylated by c-Src. Indeed, we found that Ang II induced the c-Src-mediated tyrosine phosphorylation of the beta-subunit of AP-2 (beta2-adaptin). We were able to map one of the tyrosines in beta2-adaptin and assess its role in regulating the binding of its principal partner: betaarrestin. The phosphorylation state of beta2-adaptin dictates its association profile with betaarrestin: when phosphorylated it reduces its binding to betaarrestin. Finally, we proposed a model for AT1R internalization. Overall, these studies are significant because they allow a better understanding of the underlying mechanism that regulates the initial steps of clathrin-coated vesicle endocytosis of AT1R.
Armando, Sylvain. "Structure quaternaire des récepteurs de chimiokines CXCR4 et CCR2 et interaction avec leur effecteurs." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20208/document.
Full textG protein coupled receptors (GPCR) are the most represented cell surface receptors among vertebrates, and the major therapeutic target in humans. The initial paradigm stating a 1 :1 :1 stoichiometry for receptor :G protein :effector has evolved to a more complex model, as illustrated here with the example of the chemokine receptors CXCR4 and CCR2. Bioluminescence resonance energy transfer (BRET) was used to demonstrate that (1) CXCR4 is able to couple Gα13 instead of Gαi to promote breast cancer metastasis, (2) the multiple pathways engaged by stimulation of CXCR4 are selectively desensitized by the specific recruitment of a defined combination of proteins (GRKs and arrestins) and (3) the CXCR4 protomer plays a crucial role during Gαi engagement and β-arrestin recruitment by the CXCR4/CCR2 heterodimer upon CCR2 activation. In this last and main study, the results shown also demonstrate that CCR2 dimers could assemble with CX CR4 dimers into hetero-tetramers, and that CCR2 activation leads to a conformational change in the CXCR4 dimer. Former results showing cooperativity and asymmetric activation of a simple CXCR4/CCR2 heterodimer could then be applied to a tetramer. To conclude, the work done during this thesis demonstrates a more sophisticated regulation of chemokine receptors than previously suspected at 3 different levels: quaternary structure of the protomers, G protein signalling, and signalling termination
RAZAGHI, AHMAD. "Les proteines apparentees a l'antigene-s/arrestine : une nouvelle famille de proteines." Paris 6, 1992. http://www.theses.fr/1992PA066592.
Full textLake, David Jonathan. "A human alpha-arrestin protein with a potential role in cargo protein trafficking within the endocytic system." Thesis, University of Nottingham, 2013. http://eprints.nottingham.ac.uk/13335/.
Full textWitty, Marie-France. "Role of the adaptor protein, beta-arrestin1, in the Notch signaling pathway." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/446.
Full textHirata, Cristiane Lumi. "Thioredoxin interacting protein (Txnip) forms redox sensitive high molecular weight nucleoprotein complexes." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/264647.
Full textGoh, Poh. "Roles of protein kinase C and arrestin in migration of cells via CXCR4/CXCL12 signalling axis." Thesis, University of East Anglia, 2018. https://ueaeprints.uea.ac.uk/67806/.
Full textLortie, Karine. "The growth-arrest-specific protein gas7 potentiates neuronal differentiation." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26701.
Full textRao, Deepa Prema. "The role of growth arrest-specific 6 in venous thromboembolism /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112349.
Full textMethods. To analyze the association between gas6 and venous thromboembolism, a highly specific ELISA method was used to measure plasma gas6 levels in 306 patients with a history of deep-vein thrombosis (DVT) and 89 control volunteers. Medication history, comorbid conditions and DVT characteristics were documented for the purposes of statistical analyses. Median gas6 levels were compared between the subgroups, and prevalence rate ratios were calculated. Human umbilical vein endothelial cells were used to measure the effect of gas6 treatment on the expression of various mediators of coagulation. Murine thrombosis models were developed to serve as in vivo models for thrombosis.
Results. The median levels of gas6 were 28.21 ng/ml in patients compared to 26.15 ng/ml in controls (p=0.01). After adjustment for age, sex, comorbidity and medications, DVT patients had a PRR of 2.5 (95% CI 1.36 to 4.61, p=0.003) compared with controls. Within the DVT subgroup, median gas6 levels were significantly higher in those with cancer-associated (vs. unprovoked or secondary) DVT (p<0.001) and in those with more extensive DVT (p=0.037), while levels were significantly lower in those taking warfarin (vs. no warfarin) (p=0.03). Preliminary results with endothelial cell cultures are inconclusive with regards to the effect of gas6 on endothelium derived mediators of coagulation.
Conclusions. Elevated plasma gas6 is associated with venous thromboembolism. The etiology of the clot influences detected levels of gas6, with the highest levels seen in cancer-patients. Furthermore, increasing clot burden correlates with elevated levels of gas6. A mechanistic explanation for how gas6 modulates this association is in its preliminary stages, and is worth pursuing.
Crosby, Meredith Ellen. "E2F4 is a critical molecule involved in the cell cycle arrest reponse following ionizing radiation." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1136934596.
Full text[School of Medicine] Department of Environmental Health Sciences. Includes bibliographical references. Available online via OhioLINK's ETD Center.
Mariggio, Stefania Pasqua. "Regulation of immune receptor functional responses by G protein-coupled receptor kinases (GRKs) and arrestins." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343747.
Full textRaehal, Kirsten Michele. "Opioid-Induced Side Effects in Beta-arrestin2 adn G Protein-Coupled Receptor Kinase Knockout Mice." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1236884585.
Full textRaehal, Kirsten M. "Opioid-induced side effects in beta-arrestin2 and G protein-coupled receptor kinase knockout mice." Columbus, Ohio : Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1236884585.
Full textKemp, Hilary A. "A complex of six FAR proteins required for pheromone arrest and mating /." view abstract or download file of text, 2003. http://wwwlib.umi.com/cr/uoregon/fullcit?p3113011.
Full textTypescript. Includes vita and abstract. Includes bibliographical references (leaves 94-104). Also available for download via the World Wide Web; free to University of Oregon users.
Schmid, Cullen L. "Differential regulation of serotonin 2A receptor responsiveness by agonist-directed interactions with beta-arrestin2." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1300287547.
Full textBhattacharya, Sarbani [Verfasser]. "Structural and functional studies of growth arrest and DNA-damage proteins / Sarbani Bhattacharya." Berlin : Freie Universität Berlin, 2010. http://d-nb.info/1023959607/34.
Full textSehat, Bita. "SUMO and ubiquitin; the yin and yang of IGF-1R function /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-360-3/.
Full textMorais, Carla Patrícia Amorim Carneiro de. "A atividade do NHE3 em túbulo proximal é inibida pela sinalização enviesada do receptor de angiotensina II tipo 1/beta-arrestina." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5166/tde-20042016-113857/.
Full textCell surface receptors mediate most of our physiological responses to an array of stimulus. The triggering of the angiotensin II type I (AT1) receptor signaling is the major control point in the regulation of the ultimate effects of the peptide hormone angiotensin II (Ang II) on its target tissue. In the kidney physiological concentrations of Ang II upregulate the activity of proximal tubule Na+/H+ exchanger isoform 3 (NHE3). This effect is crucial for maintenance of extracellular fluid volume homeostasis and blood pressure. Recent findings have shown that selective activation of the betaarrestin-biased AT1 receptor signalingpathway induces diuresis and natriuresis independent of G-protein mediated signaling. This study tested the hypothesis that activation of this AT1 receptor/beta-arrestin signaling inhibits NHE3 activity in proximal tubule as well as investigate the underlying molecular mechanisms mediating this effect. To this end, we determined the effects of the compound TRV120023, which binds to the AT1R, blocks G protein coupling, and stimulates beta-arrestin signaling, on NHE3 function in vivo and in vitro. NHE3 activity was measured in both native proximal tubules, by stationary microperfusion, and in opossum proximal tubule (OKP) cells, by Na+-dependent intracellular pH recovery. Our results showed that 10-7 MTRV120023 remarkably inhibited proximal tubule NHE3 activity both in vivo and in vitro, and the effect was completely abolished in OKP cells silenced for beta-arrestin 1 and 2 by small interference RNA. Additionally, stimulation of NHE3 by Ang II was completely suppressed by TRV120023 both in vivo as well as in vitro. Inhibition of NHE3 activity by TRV120023 was associated with a decrease in NHE3 surface expression in OKP cells and with a redistribution from the body to the base of the microvilli in the rat proximal tubule. The decreased surface NHE3 in OKP cells was associated with an increase in NHE3 internalization via clathrin mediated endocytic. Beta-arrestin mediated NHE3 inhibition did not involve AT2 receptor, cAMP/ PKA, Akt and ERK1/2 signaling. These findings indicate that biased signaling of the AT1 receptor/beta-arrestin pathway inhibits NHE3 activity in the proximal tubule at least in part due to changes in NHE3 subcellular localization
Costa, Mariana Fernandes Alves. "Molecular remodelling of the spindle architecture during metaphase arrest in oocytes." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31255.
Full textAzoulay, Eric. "Induction of apoptosis or cell cycle arrest by two human wildtype variants of the p53 protein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0031/MQ64313.pdf.
Full textZhang, Yuan. "An investigation of p53’s differential activation of cell cycle arrest and apoptosis." Thesis, Curtin University, 2008. http://hdl.handle.net/20.500.11937/1577.
Full textMuchhala, Karan Hitesh. "An investigation on the role of β-arrestin 2, protein kinase C and sex on the mechanism of morphine tolerance in the mouse ileum." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/6074.
Full textMayall, Stephen James. "Cyclins in the slime mould Dictyostelium discoideum." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243862.
Full textZhang, Yuan. "An investigation of p53’s differential activation of cell cycle arrest and apoptosis." Curtin University of Technology, School of Pharmacy, 2008. http://espace.library.curtin.edu.au:80/R/?func=dbin-jump-full&object_id=118347.
Full textSivko, Gloria S. BS DV M. "Characterization and regulation of C/EBPδ in human mammary epithelial cell G0 growth arrest." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1082580020.
Full textAikio, M. (Mari). "Novel roles for basement membrane collagens:isoform-specific functions of collagen XVIII in adipogenesis, fat deposition and eye development, and effects of the collagen IV-derived matricryptin arresten on oral carcinoma growth and invasion." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526203188.
Full textTiivistelmä Kollageeni XVIII on tyvikalvojen proteoglykaani ja yksi harvoista evoluutiossa konservoituneista kollageeneista. Se esiintyy elimistössä kolmena isomuotona, joiden biologiset tehtävät ovat vielä jokseenkin epäselviä. Tässä tutkimuksessa selvitettiin kollageeni XVIII:n isomuotojen fysiologista merkitystä hyödyntäen uusia hiirilinjoja, joilta kollageeni XVIII:n lyhyt tai kaksi pisintä varianttia oli geneettisesti inaktivoitu. Poistogeenisten hiirimallien rinnalle tehtiin kaikille varianteille yhteistä trombospondiini-1 (Tsp-1)-domeinia yli-ilmentävä hiirilinja. Tämän väitöskirjatutkimuksen avulla saatiin uutta tietoa kollageeni XVIII:n ja etenkin sen lyhimmän variantin tärkeästä roolista silmässä. Aikaisemmat tutkimukset ovat osoittaneet kollageeni XVIII:n puutteen häiritsevän silmän verkkokalvon verisuonituksen normaalia kehittymistä. Tässä työssä havaittiin, että pelkästään lyhyen isomuodon puute riitti altistamaan hiiret muutoksille verkkokalvon suonituksessa. Tsp-1-osan ylimäärän havaittiin lisäksi alistavan hiiret muutoksille silmän rakenteessa, mahdollisesti häiritsemällä silmässä jo olemassa olevan kollageeni XVIII:n toimintaa. Tässä työssä havaittiin myös uusi yhteys kollageeni XVIII:n ja rasvasolujen kypsymisen välillä. Verrokkihiiriin verrattuna muodostuvan rasvakudoksen havaittiin jäävän merkittävästi vähäisemmäksi poistogeenisillä hiirillä, joilta kollageeni XVIII:n pitkät isomuodot olivat geneettisesti inaktivoitu. Heikentynyt rasvakudoksen muodostuminen lisäsi triglyseridien kertymistä hiiren verenkiertoon ja maksaan. Tutkimustulos on merkittävä avaus soluväliaineen merkityksestä rasva-aineenvaihdunnalle ja kannustaa lisätutkimuksilla selvittämään, onko kollageeni XVIII:lla yhteys myös ihmisen metaboliseen oireyhtymään. Soluväliaineen komponenttien entsymaattinen muokkaus tuottaa usein molekyylejä, joilla on uusia isäntämolekyyleistä poikkeavia ominaisuuksia. Tässä työssä tutkittiin yhden tällaisen molekyylin, tyvikalvokollageenin IV hajoamistuotteen, arrestenin, suoria vaikutuksia syöpäsoluille. Arrestenin tiedettiin entuudestaan estävän syöpäkasvainten verisuonten uudismuodostusta koe-eläimillä. Työssä osoitettiin, että arresten vaikutti endoteelisolujen lisäksi myös itse syöpäsoluihin estäen niiden lisääntymistä ja vähentäen niiden elinkykyä ja liikkuvuutta, mikä tekee arrestenista entistä houkuttelevamman ehdokasmolekyylin lääkekehitystyöhön
Fujinaga, Takuji. "Isoflurane inhalation after circulatory arrest protects against warm ischemia reperfusion injury of the lungs." Kyoto University, 2007. http://hdl.handle.net/2433/135895.
Full textHouri, Nadia. "Study of ERK12 MAP kinases activation by the bradykinin type 2 receptor : characterization of beta-arrestin scaffolding function in the temporal regulation of ERK12 activation induced by the B2R." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112637.
Full textPokela, M. (Matti). "Predictors of brain injury after experimental hypothermic circulatory arrest:an experimental study using a chronic porcine model." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:951427105X.
Full textZhang, Tong. "The investigation of growth-arrest-specific 2 protein functions in cell division and its cytoskeleton binding mechanisms." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116848.
Full textLe cytosquelette participe à de nombreuses fonctions dans les cellules eucaryotes et sa bonne coordination est essentielle au bon fonctionnement de ces fonctions biologiques. Ces fonctions sont partiellement accomplies grâce aux protéines de liaisons des filaments actine-microtubule (MT). La protéine Gowth-arrest-specific (Gas) 2 a été originellement identifiée dans des fibroblastes murins en arrêt de croissance. Le fait que la protéine Gas2 contienne des domaines putatifs d'intéractions avec actine et les microtubules supporte l'hypothèse qu'elle agit comme protéine de liaison des filaments actine-microtubule. Cependant, les mécanismes que Gas2 utilise pour interagir avec le cytosquelette et participer à la division cellulaire ne sont pas connus. Cette thèse répond à ces questions.Dans le deuxième chapitre, nous avons démontré que la protéine Gas2 participe à la division cellulaire de l'embryon et à la cicatrisation de la plaie de l'ovocyte chez le Xenopus laevis. Nous avons trouvé que la protéine entière (FL) Gas2 et son domaine d'intéraction avec les microtubules, mais pas son domaine d'intéraction avec actine homologue a calponine (CH), inhibent la division cellulaire et résultent en la formation de cellules multinucléées. Nous déduisons du fait que le domaine de Gas2 puisse causer un arrêt de la division cellulaire à lui seul que la protéine entière FL-Gas2 fonctionne grâce à l'intéraction avec les microtubules. Pour étudier comment Gas2 induit l'arrêt de la division cellulaire, nous avons utilisé un essai d'induction de contraction par cicatrisation et démontré que FL-Gas2 stabilise les microtubules. Dans le troisième chapitre, nous avons étudié en détails comment la protéine FL-Gas2 interagit avec le cytosquelette dans les cellules HeLa. Le domaine de Gas2 change dramatiquement la morphologie des microtubules, celles-ci forme un réseau de boucles longues et regroupées. La protéine FL-Gas2 favorise la polymérisation des microtubules et change leur comportement dynamique. Il existe trois sites de phosphorylation par la protéine kinase C (PKC) dans FL-Gas2. Des points de mutations imitant la phosphorylation de ces trois sites ont démontré que les trois sites participent aux changements de fonctionnalité de FL-Gas2. La chromatographie par exclusion de taille a démontré que FL-Gas2 forme un complexe dynamique qui doit jouer un rôle important dans l'intéraction de la protéine avec le cytosquelette.En conclusion, nos résultats suggèrent que la protéine FL-Gas2 non-phosphorylée forme un complexe pour regrouper les microtubules, et qu'elle crée une liaison entre F-actine et les microtubules lorsqu'elle est phosphorylée. Nous formulons hypothèse que Gas2 agit en intéragissant et en regroupant les microtubules ce qui cause un arrêt de la division cellulaire.
Wong, Kam-wai, and 黃錦偉. "The molecular mechanism of mitotic arrest induced by a novel diterpenoid pseudolaric acid B and a novel gene encoding RNA-bindingprotein 22." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37679090.
Full textWong, Kam-wai. "The molecular mechanism of mitotic arrest induced by a novel diterpenoid pseudolaric acid B and a novel gene encoding RNA-binding protein 22." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37679090.
Full textTheuer, Stefanie [Verfasser]. "Die Rolle von growth arrest specific protein 6 im Aldosteron induzierten Endorganschaden : Untersuchungen an einem Knockout-Mausmodell / Stefanie Theuer." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1042658005/34.
Full textChen, Dong. "Function of Insulin-like Growth Factor Binding Protein 7 (IGFBP7) in Hepatocellular Carcinoma." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2821.
Full textInamdar, Kaushik. "Role of I-BAR proteins and membrane curvature in HIV-1 assembly and release." Thesis, Montpellier, 2020. http://www.theses.fr/2020MONTT032.
Full textDuring the HIV assembly and budding, the plasma membrane undergoes a curvature driven by HIV-1 Gag self-assembly at the assembly site towards the exterior of the cell. However, the multimerization of Gag may not be sufficient and Gag may need to recruit cell factors for inducing local membrane curvature. We recently reported that the HIV-1 Gag particle release was dependent on the activation of the signalling pathway Rac1/IRSp53/Wave2/Arp3 in Jurkat T cells and primary blood lymphocytes. This cellular complex, when activated, is recruited to the cell plasma membrane and promotes the recruitment of actin branching, actin polymerisation and membrane remodelling in lamellipodia. In particular, the protein IRSp53 contains an I-BAR domain capable of inducing membrane curvature via the recognition of the plasma membrane phospholipide PI(4,5)P2. This phospholipid is also specifically recognized by the N-terminal Matrix domain of Gag and is a lipidic cofactor of Gag targeting to the plasma membrane and of HIV-1 assembly. This research project aimed at characterizing the cellular and molecular mechanisms of IRSp53 involvement in HIV-1 Gag assembly in CD4 T cells and HEK293T cells. Our results show that IRSp53 is associated with viral particles and that its knockdown by siRNA decreases HIV-1 release in T lymphocytes and HEK293 T cells. Electron microscopy of cells knocked down for IRSp53 revealed a striking phenotype of viral buds arrested at an early stage of assembly. Immunoprecipitation of IRSp53 showed a p6 independent pulldown of HIV-1 Gag, indicating intracellular complexing of Gag and IRSp53. Cellular fractionation and membrane flotation showed that IRSp53 recruitment to cellular membrane doubles upon expression of HIV-1 Gag. Dual colour single molecule PALM/STORM microscopy and subsequent analyses showed IRSp53 in close proximity to Gag clusters. We also found specific incorporation of IRSp53 in HIV-1 Gag particles as compare to other I-BAR proteins, a phenomenon dependent on its IBAR domain. As the I-BAR domain is involved in membrane curvature, we then probed this aspect of IRSp53 involvement in HIV-1 assembly. Analysis of electron microscopy images revealed a curvature defect for buds from IRSp53 knocked out cells. Concomitant studies in cell free in vitro GUV systems also indicated a role for IRSp53 induced membrane curvature in Gag membrane binding. These results affirm the essential role of IRSp53 in the early stages of HIV-1 assembly. Finally as IRSp53 is a vital player in scaffolding actin signaling proteins, we established a role for activated Rac1 in IRSp53 membrane recruitment downstream of HIV-1 Gag, and test the involvement of the RacGEF Tiam1 in HIV-1 particle production. Super resolution microscopy also reveals the presence of actin nanostructures at HIV-1 assembly sites. All these results highlight the novel and essential role of the membrane curving I-BAR protein IRSp53, and the mobilization of cortical actin, in the late phases of HIV-1 replication
Deye, Nicolas. "Cardiac Arrest-Induced Brain Injury : Diagnostic And Prognostic Values of Circulating Biomarkers." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC150.
Full textOutcome of cardiac arrest (CA) remains dramatic. To quickly diagnose the cause of CA and establish a reliable outcome prediction (prognostication) as early as possible could help to guide initial treatments. It could avoid futile treatments in patients with low chance of survival or of good neurological recovery, or conversely allow treatment optimization in patients expected to have a high likelihood of good neurological outcome. Usefulness of biomarkers to guide clinicians in finding the CA diagnosis and helping prognostication is debated. Biomarkers are considered as not sensitive and accurate enough, especially within the first hours after return of spontaneous circulation (ROSC). Their use is only recommended in prognostication for Neuron Specific Enolase (NSE) as a second line tool and after the third day from CA. Our first study confirmed that biomarkers “specific” of brain injury (S100B protein: S100 and moreover NSE) cannot sufficiently discriminate the neurological cause of CA on ICU admission. If early coronary angiogram is the standard for diagnosing a probable cardiac cause of CA, biomarkers cannot replace brain computed-tomography (CT) in CA from a neurological cause. The second study evaluated, during the 1st day after ROSC, the link between biomarkers (S100 and NSE) and 2 surrogates of brain oedema recently proposed as outcome predictors: echography of the optic nerve sheath diameter (ONSD), and grey to white matter attenuation ratio (GWR) on brain CT-scan. Even though we cannot conclude on a definitive relationship between these parameters, ONSD enlargement at day 1 was associated with specific brain damage after CA, such as brain oedema and mostly axonal injuries, as reflected by increases in NSE (on admission and at day 1) and low GWR measurements. Whereas NSE, GWR and ONSD at day 1 were correlated, S100, which is more specific of glial injuries, did not reach significance. NSE and S100 on admission, at days 1 and 2 after ROSC, as well as ONSD at day 1, were associated with survival at hospital discharge. The third study evaluated the prognostic value of several biomarkers in the early phase after CA (NSE and S100 being sampled at median 220 min after ROSC). S100, blinded to physicians, was the biomarker with the best accuracy after ICU admission to correctly predict unfavourable outcome at hospital discharge and at 3 months after CA, compared with all other biomarkers such as lactate, pH, creatinine, and especially NSE. S100 variations during the first day after admission refined prognostication. Initial S100 was an early independent predictive factor associated with unfavourable outcome at hospital discharge, with the no-flow duration, initial lactate value, initial non-shockable rhythm, and the presence of clinical seizure. According to guidelines, prognostication theoretically needs to be delayed and multimodal, biomarkers alone not being recommended especially in the early phase after CA. Biomarkers cannot seem to be an alternative option compared to imaging to precisely diagnose the CA cause. By contrast, some biomarkers, such as S100 after admission, could easily and specifically discriminate CA patients with certainty of unfavourable outcome. Associated with other predictive tools (clinical or using imaging), biomarkers could interestingly be incorporated in early decisional algorithms to optimally guide initial therapies. This correct patient classification could help to avoid unuseful treatments versus to maximize aggressive therapies. The choice of recommended servo-controlled targeted temperature management devices, very efficient but invasive and expensive, or the indication -or not- of a cardio-circulatory assist device implementation should be guided in the early stage after ROSC using this simple strategy of patient selection
Roopchand, Diana Elizabeth. "Human adenovirus E4orf4 protein induces premature mitotic arrest by a PP2A-dependent mechanism leading to cell death in Saccharomyces cerevisiae." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86049.
Full textE4orf4 expression can induce high levels Clb2-Cdc28 activity and mitotic arrest in a Cdc55-dependent manner. Since E4orf4 targets only the Cdc55-containing pool of PP2A, the E4orf4-induced mitotic arrest suggests that PP2A-Cdc55 plays a direct role in regulating exit from mitosis. Two anaphase-promoting complexes (APCs) control mitotic exit, APCCdc20 and APCHct1. We find that E4orf4 induces premature APCCdc20 activity resulting in the premature degradation of Pds1 and Scc1 in a Cdc55-dependent manner. In contrast, E4orf4 did not induce APCHct1 as evidenced be the stability of its substrates, Cdc20, Clb2 and Cdc5 as well as the hyperphosphorylation of Hct1. E4orf4 prevents Cdc55-containing PP2A complexes from localizing normally, another mechanism by which E4orf4 may modulate PP2A activity towards substrates. We propose that E4orf4 promotes mitotic arrest by acting as a Cdc55-specific inhibitor of PP2A and that PP2A plays a role in controlling the timing of anaphase by regulating APCCdc20 activity.
Guo, Yang. "Overexpression of Heat-Shock Protein 27 (HSP27) increases gemcitabine sensitivity in pancreatic cancer cells through s-phase arrest and apoptosis." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-176979.
Full textHassumani, Daniel O. "Expression of Growth Arrest and DNA Damage Protein 45-alpha (gadd45-alpha) and the CCAAT/enhancer binding protein-delta (C/EBP-delta) in Fishes Exposed to Heat and Hypoxia." Thesis, Portland State University, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=1536122.
Full textThe cellular stress response (CSR) is one of the most highly conserved mechanisms among all organisms. Cellular stress can be defined as damage or the threat of damage to proteins, macromolecules and/or DNA. The response to damage can involve cell cycle regulation, protein chaperoning, DNA repair or, if macromolecular damage is too severe, apoptotic mechanisms can be initiated. This thesis details experiments that were designed to examine the cellular response to non-lethal environmental stressors at the protein level, using two fish species as study models. Two proteins that can cause cell cycle arrest and apoptosis mechanisms were examined. Expression of the CCAAT enhancer binding protein-delta (C/EBP-δ) was examined in the zebrafish, Danio rerio, exposed to acute, non-lethal hypoxic conditions. While C/EBP-δ was expressed constitutively in control individuals during all time points, exposure to hypoxic conditions did not have a consistent significant effect on C/EBP-δ expression (two-way ANOVA, P>0.05) in zebrafish white muscle tissue. In a second study, the expression of the growth arrest and DNA damage 45-alpha protein (gadd45-α), a mediator of cell cycle arrest and perhaps apoptosis was examined in heat-stressed liver tissue of an extremely cold-adapted Antarctic fish, Trematomus bernacchii. Gadd45-α levels were higher in fish exposure to 2°C across all time points (one-way ANOVA; P<0.05). The findings in these two studies expand our understanding of the CSR and how two genes that are involved in cell cycle regulation respond to acute, non-lethal environmental stress.
Hassumani, Daniel Omar. "Expression of Growth Arrest and DNA Damage Protein 45-alpha (gadd45-alpha) and the CCAAT/enhancer binding protein-delta (C/EBP-delta) in Fishes Exposed to Heat and Hypoxia." PDXScholar, 2013. https://pdxscholar.library.pdx.edu/open_access_etds/943.
Full textSercovich, Mark J. "Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr)-mediated cell cycle arrest : an analysis of current mechanistic models /." Download the thesis in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/sercovich2006.pdf.
Full textMagnin, Florence Magnin Florence. "How adeno-associated virus Rep78 relocalises Cdc25B to arrest the cell cycle : the multiple interactions of Rep78 with cellular regulatory, replication and rcombination proteins /." [S.l.] : [s.n.], 2009. http://library.epfl.ch/theses/?nr=4486.
Full textBrignole, Claudine. "The adenovirus E4orf4 protein induces G2 / M arrest and cell death by inhibiting PP2A phosphatase activity regulated by the B Alpha subunit /." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81604.
Full textLabasque, Marilyne. "La calmoduline, un partenaire du récepteur 2C de la sérotonine essentiel à la signalisation indépendante des protéines G et dépendante des arrestines du récepteur." Montpellier 1, 2008. http://www.theses.fr/2008MON1T016.
Full textByrne, Tara. "The evaluation of the effects of the Mitotic Arrest Deficiency Protein 2 (MAD2) and the miR-433 microRNA on chemoresistance and cancer prognosis." Thesis, Queen's University Belfast, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.725493.
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