Дисертації з теми "Membrane protein band 3"
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Boulter, Jonathan Michael. "Structural and functional studies of the erythrocyte anion exchanger, band 3." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297079.
Повний текст джерелаYoung, Mark. "Studies of the transmembrane domain of the human erythrocyte anion exchanger (band 3)." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340324.
Повний текст джерелаMalik, Saira. "Protein-protein and protein-lipid interactions of band 3 in native and model membranes." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302943.
Повний текст джерелаParker, Mark D. "Expression and anion transport studies on the human erythrocyte anion exchange protein (AE1, band 3) in the yeast Saccharomyces cerevisiae." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310589.
Повний текст джерелаStauffer, Kathrin. "On the structure and function of membrane-integrated segments of the human erythrocyte band 3 protein /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
Повний текст джерелаTaylor, Andrew Mark. "Biophysical studies on the human erythrocyte anion transporter, band 3." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360571.
Повний текст джерелаClague, M. J. "A rotational dynamic study of Erythrocyte membrane proteins : Cytoskeletal restraints on band 3 and its aggregation by positively charged species." Thesis, University of Essex, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381251.
Повний текст джерелаChe, Alexis Pun Kit. "Studies of band 3 rotational mobility in normal and ovalocytic human red blood cell membranes by transient dichroism." Thesis, University of Essex, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241212.
Повний текст джерелаBruce, Lesley J. "A study of human erythrocyte band 3 variants." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240590.
Повний текст джерелаWang, Lin. "Complementation and membrane assembly studies of human erythrocyte anion exchanger (AE1, band 3)." Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388102.
Повний текст джерелаDenbow, Cynthia J. "Membrane Domain of Plant 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase: Targeting, Topology, and Function." Diss., Virginia Tech, 1997. http://hdl.handle.net/10919/30472.
Повний текст джерелаPh. D.
Schischmanoff, Olivier. "Etude de l'interaction ankyrine-protéine bande 3 dans les sphérocytoses héréditaires." Paris 5, 1993. http://www.theses.fr/1993PA05P180.
Повний текст джерелаWu, Hao. "Structural and functional characterization of scaffold protein par-3 /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20WU.
Повний текст джерелаAdams, Charlotte Lynne 1971. "Tandem MS/MS analysis of band 3 protein from young and old erythrocytes." Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282574.
Повний текст джерелаNilsson, Johan. "Membrane protein topology : prediction, experimental mapping and genome-wide analysis /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-963-3/.
Повний текст джерелаMcPhee, Helen Kennedy. "A study of the membrane binding properties of the matrix protein from human respiratory syncytial virus." Thesis, Durham University, 2009. http://etheses.dur.ac.uk/3/.
Повний текст джерелаChristians, Arne [Verfasser], and Stefan [Akademischer Betreuer] Wiemann. "Funktionelle Charakterisierung des putativen Tumorsuppressors "Epithelial Membrane Protein 3" / Arne Christians ; Betreuer: Stefan Wiemann." Heidelberg : Universitätsbibliothek Heidelberg, 2014. http://d-nb.info/1180300955/34.
Повний текст джерелаJones, Graham K. "Expression and anion transport studies on the human erythrocyte anion exchange protein (AE1, band 3)." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245676.
Повний текст джерелаRamakrishnan, Sarathiraja. "Encapsulation of omega-3 fatty acids by premix membrane emulsification." Doctoral thesis, Universitat Rovira i Virgili, 2013. http://hdl.handle.net/10803/145770.
Повний текст джерелаEl aceite de pescado es altamente valorado en la industria alimentaria por su demostrada actividad en la prevención y tratamiento de numerosas patologías, asociada a su contenido en ácidos grasos omega-3. La incorporación de aceite de pescado en alimentos presenta algunas dificultades relacionadas con su rápida oxidación y su característico aroma y sabor. La encapsulación del aceite de pescado retrasa la oxidación y permite enmascarar sus propiedades sensoriales. Tradicionalmente, la encapsulación se lleva a cabo combinando una etapa de emulsificación seguida de secado por atomización. El objetivo principal del trabajo es estudiar el efecto del método de emulsificación y la formulación de la emulsión y las microcápsulas en los parámetros físico-químicos más relevantes de las microcápsulas. En este proyecto se combina por primera vez la emulsificación por membranas con el secado por atomización para obtener microcápsulas de aceite de pescado aplicables a la industria alimentaria. Los resultados muestran una clara mejora en la eficiencia de encapsulación del aceite cuando se reduce el tamaño de gota de la emulsión y se incrementa la cantidad de material de pared de las microcápsulas. La combinación de un polisacárido con una proteína para la formación de la pared mejora la estabilidad oxidativa de las microcápsulas durante el almacenamiento. Por otra parte la adición de proteínas desnaturalizadas para reforzar las paredes de las microcápsulas ha resultado en una mejora de la eficiencia de encapsulación de aceite pero no ha mejora su resistencia mecánica
Kilelee, Erin M. "Modeling the interaction of the platelet microbicidal protein tPMP-1 with the cell membrane." View electronic thesis (PDF), 2009. http://dl.uncw.edu/etd/2009-3/r3/kileleee/erinkilelee.pdf.
Повний текст джерелаDarbyson, Angie L. "ORP-3 Rescues ER Membrane Expansions Caused by the VAPB-P56S Mutation in Familial ALS." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/29054.
Повний текст джерелаWenham, Matt. "The role of Adaptor Protein 3 in cytotoxic T lymphocytes." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:1a5c1fd6-c8cc-454f-81a5-b9a5a18c1540.
Повний текст джерелаLefnaier, Wafa. "Potential Role for the Sarcolemmal Membrane Associated Protein Isoform 3 (SLMAP3) in Cardiac Remodeling Post Myocardial Infarction." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35713.
Повний текст джерелаLiu, Tina Yu. "Mechanism of endoplasmic reticulum membrane fusion mediated by the Atlastin GTPase." Thesis, Harvard University, 2014. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13064987.
Повний текст джерелаFujita, Koji. "Clostridium perfringens enterotoxin binds to the second extracellular loop of claudin-3, a tight junction integral membrane protein." Kyoto University, 2001. http://hdl.handle.net/2433/150516.
Повний текст джерелаVoss, Matthias. "Signal peptide peptidase-like 3 (SPPL3) is a type II membrane protein-selective sheddase that regulates cellular N-glycosylation." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-181243.
Повний текст джерелаIntramembranproteolyse, die hydrolytische Spaltung von Membranproteinen innerhalb ihrer Transmembrandomänen, ist ein wichtiger zellulärer Prozess, der in allen Reichen der Lebewesen konserviert ist. Die Intramembranproteolyse wird von unterschiedlichen Klassen von polytopen Membranproteinen, den Intramembranproteasen, ausgeführt, die eine hydrophile Proteinumgebung innerhalb des hydrophoben Bereichs der Membran bilden. In dieser Umgebung finden sowohl Membranproteinsubstrate als auch Wassermoleküle Platz und Hydrolyse der Peptidbindung wird durch die Intramembranproteasen katalysiert. Vor allem die Aspartylintramembranproteasen haben sehr viel Aufmerksamkeit auf sich gezogen, da die Preseniline, die katalytischen Untereinheiten des γ-Sekretasekomplexes, als Schlüsselenzyme in der Pathophysiologie der Alzheimer-Erkrankung identifiziert wurden. Neben den Presenilinen finden sich in Säugetiergenomen auch Presenilinhomologe, welche sowohl die Signalpeptidpeptidase (SPP) als auch SPP-ähnliche (SPP-like, SPPL) Proteasen umfassen. Aus diesen sticht die im Golgi lokalisierte Protease SPPL3 heraus, da sie in vielzelligen Tieren hochkonserviert ist und sich SPPL3-Orthologe auch in Pflanzen finden. Gleichzeitig ist SPPL3 jedoch, vor allem aufgrund der Tatsache, dass keine Substrate beschrieben wurden, bisher kaum charakterisiert. Daher war es das Ziel dieser Arbeit Substrate von SPPL3 zu identifizieren und seine physiologische Funktion(-en) aufzuklären. Im ersten Teil dieser Arbeit wurde ein erstes SPPL3-Substrat, das foamy-virale Hüllglykoprotein (FVenv), identifiziert. Dies erlaubte die proteolytische Aktivität von SPPL3 und insbesondere seine Substratselektivität sowie seine Sensitivität gegenüber Inhibitoren von Aspartylintramem- branproteasen im Detail zu untersuchen. Es konnte ebenfalls festgestellt werden, dass zwei weitere Intramembranproteasen, SPPL2a und SPPL2b, FVenv ebenfalls endoproteolytisch spalten. Vor allem SPPL2b war bereits zuvor im Detail untersucht worden und daher konnte die SPPL3- beziehungsweise SPPL2b-vermittelte Endoproteolyse von FVenv verglichen werden. Dies offenbarte eine unerwartete Eigenheit von SPPL3, welche SPPL3 deutlich von anderen Intramembranproteasen, vor allem den anderen Aspartylintramembraneproteasen, unterschiedet: SPPL3 spaltete das FVenv-Holoprotein und bedarf keinem vorherigen Zuschneiden des Substrates durch eine andere proteolytische Aktivität - ein sonst sehr verbreitetes Phänomen bei Intramembranproteasen. Im zweiten Teil sollte die physiologischen Funktion von SPPL3 untersucht werden. Dabei zeigte sich, dass Änderungen in der zellulären SPPL3-Aktivität große Auswirkungen auf die Zusammensetzung der N-Glykane auf endogenen zellulären Glykoproteinen haben. SPPL3- Überexpression ging mit einer Reduktion des Molekulargewichts untersuchter Glykoproteine, einem so genannten Hypoglykosylierungsphänotyp, einher, während der Verlust der SPPL3- Expression im Zellkulturmodell aber auch in vivo in einem Hyperglykosylierungsphänotyp resultierte. Dies führte zur Identifizierung von glykanmodifizierenden Enzymen im Golgi wie beispielsweise GnT-V und β3GnT1 als physiologische SPPL3-Substrate. Verlust oder Reduktion der SPPL3-Expression führte zu einer starken intrazellulären Akkumulation dieser Substrate, was die unter diesen Bedingungen beobachtete umfassendere N-Glykan- ausarbeitung sowie den Hyperglykosylierungsphänotyp erklärte. Gleichzeitig wurde die Sekretion dieser Enzyme unter diesen Bedingungen stark beeinträchtigt. Zusammen mit weiteren Beobachtungen wie der Bestimmung der SPPL3-Schnittstelle im Bereich der Transmembrandomäne von GnT-V zeigte diese Studie, dass die von SPPL3 vermittelte Intramembranproteolyse solcher glykan-modifizierenden Enzyme deren Ektodomainen freisetzt und SPPL3 folglich auf diese Weise das intrazelluläre Reservoir aktiver glykan-modifizierender Enzyme kontrolliert. Hervorzuheben ist dabei, dass diese Erkenntnis in guter Übereinstimmung mit den für FVenv gemachten Beobachtungen steht. Dies legt wiederum nahe, dass SPPL3 in funktioneller Hinsicht mit einer klassischen Sheddase oder einer Rhomboidprotease gleichgestellt ist, sich jedoch von allen anderen charakterisierten Aspartylintramembranproteasen in Säugetieren unterscheidet. Um herauszufinden, ob diese Beobachtungen auch auf globaler zellulärer Ebene Bestätigung finden, wurde eine Proteomanalyse im dritten Teil dieser Arbeit durchgeführt, um das SPPL3-Degradom in HEK293-Zellen unter Überexpressionsbedingungen zu definieren. Dies führte einerseits zur Identifizierung vieler weiterer neuer, zumeist im Golgi lokalisierter SPPL3-Substratkandidaten und legte andererseits unter physiologischen Gesichtspunkten nahe, dass SPPL3 sehr mit der Funktion des Golgi-Apparats verwoben ist. Andererseits unterstützten diese Ergebnisse sehr deutlich die formulierte Hypothese, dass SPPL3 als zelluläre Typ-II-Membranprotein-selektive Sheddase agiert. Zusammengefasst liefert diese Arbeit die erste ausführliche Charakterisierung der Intramem- branprotease SPPL3. SPPL3 zeigt erhebliche Unterschiede zu anderen Aspartylintramembran- proteasen und erweist sich damit als bedeutende zelluläre Sheddase mit einer auffälligen Selektivität für Typ-II-orientierte, im Golgi lokalisierte Membranproteine. Produkte der Endoproteolyse dieser Golgi-Proteine werden sekretiert und/oder werden möglicherweise intrazellulär degradiert, was wiederum ihre eigentliche intrazelluläre Funktion beeinträchtigt. Folglich kontrolliert SPPL3 indirekt die Proteinglykosylierung im Golgi-Apparat.
Beuming, Thijs. "Structure/function studies of membrane proteins : from molecular modeling and ligand binding to protein-protein interactions of the dopamine transporter /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1432803991&sid=3&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Повний текст джерелаKimura(Takemoto), Sayaka. "Molecular cloning and characterization of CLICK-3/CaMKIγ, a novel membrane-anchored neuronal Ca[2+]/calmodulin-dependent protein kinase (CaMK)". Kyoto University, 2003. http://hdl.handle.net/2433/148486.
Повний текст джерела0048
新制・課程博士
博士(医学)
甲第10449号
医博第2648号
新制||医||844(附属図書館)
UT51-2003-T275
京都大学大学院医学研究科脳統御医科学系専攻
(主査)教授 月田 承一郎, 教授 中西 重忠, 教授 武藤 誠, 教授 成宮 周
学位規則第4条第1項該当
Adhikari, Anirban. "Regulation of guanine nucelotide exchange in inhibitory G protein alpha subunit by activator of G protein signaling 3 and novel regulatory peptides." Embargoed access until after 12/19/2006, 2005. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=114.
Повний текст джерелаBraun, Anja Catharina [Verfasser], and Monilola [Akademischer Betreuer] Olayioye. "Regulation of endocytic membrane trafficking by the GTPase-activating protein Deleted in Liver Cancer 3 (DLC3) / Anja Catharina Braun. Betreuer: Monilola Olayioye." Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2015. http://d-nb.info/1071089188/34.
Повний текст джерелаVoss, Matthias [Verfasser], and Christian [Akademischer Betreuer] Haass. "Signal peptide peptidase-like 3 (SPPL3) is a type II membrane protein-selective sheddase that regulates cellular N-glycosylation / Matthias Voss. Betreuer: Christian Haass." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1069743631/34.
Повний текст джерелаAinsworth, Julia. "Comparison of p53 and MAGI-3 regulation mediated by the E6 protein from high-risk human papillomavirus types 18 and 33." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112368.
Повний текст джерелаIn vivo and in vitro results indicated that E6 from HPV types 18 and 33 interacted similarly with p53 although, variants of the HPV-33 E6 prototype demonstrated interesting disparities. Of note was HPV-33 E6 variant 2, which degraded p53 more efficiently than prototype HPV-33 E6 and HPV-18 E6. The E6 protein from HPV types 18 and 33 also potently degraded MAGI-3 via a different pathway than that used for p53. Specifically, proteasome inhibition did not interfere with MAGI-3 degradation and MAGI-3 was not ubiquitinated in the presence of the E6 protein.
Therefore, the results described herein enhance our understanding of high-risk HPV type 33 E6 and the E6-MAGI-3 interaction.
Zamzami, Omar M. "Epstein-Barr Virus (EBV) latent membrane protein 1 (LMP1) peptides as inducers of regulatory cells to treat autoimmune haemolytic anaemia." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources. Online version available for University member only until May, 2014, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=59565.
Повний текст джерелаSiebertz, Hanna Margarete [Verfasser], Stefan [Akademischer Betreuer] Gründer, and Gerhard [Akademischer Betreuer] Müller-Newen. "Approach to the structural basis of silencing of acid-sensing ion channel 3 by the integral membrane protein stomatin / Hanna Margarete Siebertz ; Stefan Gründer, Gerhard Müller-Newen." Aachen : Universitätsbibliothek der RWTH Aachen, 2019. http://d-nb.info/1195237464/34.
Повний текст джерелаAlves, Kelly Cristina Nascimento. "Contribuições ao estudo da não-idealidade de soluções proteicas." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/3/3137/tde-29072013-161832/.
Повний текст джерелаThe study of protein solutions aiming at the modeling and simulation of downstream processes entails the study of non-ideality (in thermodynamic sense) of these solutions. For systems wherein the protein concentration is low a situation often encountered in these processes the most important technique to experimentally evaluate this non-ideality is the determination of the osmotic pressure generated by the protein in solution. Thus, the objectives of this work were: to study the influence of co-solvents on the osmotic pressure of protein solutions, to verify the absence of change in the secondary and tertiary structure of proteins in these solutions, and to thermodynamically model the obtained osmotic pressure data. The osmotic pressure was directly measured through membrane osmometry, using protein-free reference solutions with the same pH and co-solvent concentration. The data of osmotic pressure were obtained as a function of protein concentration for five different proteins (bovine serum albumin, human immunoglobulin G, ovalbumin, - lactoglobulin and lysozyme) in solution with co-solvents such as polyethylene glycol (of various chain sizes) and salts (ammonium sulfate, sodium sulfate and sodium chloride). Each data set was obtained at constant pH and co-solvent concentration. It was observed that the presence of co-solvents do shift the osmotic pressure, but this effect is dependent on the protein, the co-solvent and its concentration, and the solution pH. Measurements of fluorescence and circular dichroism of these proteins confirmed that they maintain their structure unchanged in the media, which corroborates the use of volumetric equations of state with constant parameters. The osmotic pressure data as a function of protein concentration were correlated using a osmotic equation of state comprising a repulsive term of adhesive hard spheres and a zero-order perturbation term (random approximation). The proposed model, though simple, was sufficient to properly correlate the experimental behavior.
Hallstrom, Kelly N. "The Epithelial Transmembrane Protein PERP Is Required for Inflammatory Responses to S. typhimurium Infection: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/807.
Повний текст джерелаHallstrom, Kelly N. "The Epithelial Transmembrane Protein PERP Is Required for Inflammatory Responses to S. typhimurium Infection: A Dissertation." eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/807.
Повний текст джерелаDi, Guilmi Anne-Marie. "Étude de l'interaction de l'adénovirus humain de sérotype 3 avec les cellules HeLa." Université Joseph Fourier (Grenoble ; 1971-2015), 1994. http://www.theses.fr/1994GRE10058.
Повний текст джерелаHierso, Régine. "Implication du stress oxydant dans la physiopathologie de la drépanocytose : crises vaso-occlusives, taux d'anticorps anti-bande 3 et oxydation du globule rouge." Thesis, Antilles, 2015. http://www.theses.fr/2015ANTI0045/document.
Повний текст джерелаBesides the primary defect of sickle cell disease, hemoglobin S (HbS) polymerization, other abnormal processes may contribute to the development of an inflammatory response and to an oxidative stress caused by traumatic hypoxia-reperfusion and autoxidation of HbS. The exacerbation of oxidative stress seems to participate actively in the pathophysiology of the disease and play a role in vaso-occlusive crisis (VOC). The aim of this thesis was to document the deleterious effects of oxidative stress on the red blood cell and its impact in the development of VOC. First, we have evaluated the impact of tert-butyl hydroperoxide-induced oxidative stress on blood rheology of SS and SC sickle cell patients. We have shown that sickle red blood cells (SS RBC) produce more free radicals in the presence of tert-butyl hydroperoxide (TBHP) than control subject red blood cells (AA RBC). Furthermore, SS RBC have a decreased anti-oxidant defense system. Induction of oxidative stress increases the rheological alterations already present in sickle cell patients (ie, decreased deformability, reduced aggregation, increased disaggregation threshold). In control subjects, oxidative stress induces an altered hemorheological profile close to that already present in sickle cell patients. These results suggest that oxidative stress by modulating the hemorheological abnormalities associated with sickle cell disease, could be one of the factors promoting the occurrence of sickle cell complications. Then, we have studied the impact of oxidative stress in the development of VOC, analyzing blood samples from SS patients in crisis and at steady state. 1) We have tested the hypothesis that the protein band 3 of RBC, is a major target of reactive oxygen species, which cause the appearance of senescence epitopes of this protein recognized by auto anti-band 3 antibodies; 2) We have evaluated pro- and anti-oxidants molecular and cellular markers; 3) We have studied the evolution of hemorheological parameters; 4) We have explored the activity of the autonomic nervous system, seen as a potential marker of severity. Our results show during VOC: 1) an exacerbation of the oxidative stress; 2) a decrease in anti-band 3 antibodies levels and an increase in the plasma concentration of erythrocyte microparticles, suggesting that these two processes are linked to the clustering phenomenon of band 3 protein triggered by oxidative stress; 3) an exacerbation of hemorheological abnormalities resulting in a reduction of SS RBC deformability, increased aggregation and disaggregation threshold; 4) an impairment of the autonomic nervous system marked by a withdrawal of parasympathetic activity and this imbalance is accentuated during VOC. This work allows a better understanding of the complex pathophysiology of sickle cell disease, highlighting the impact of oxidative stress in the development of VOC, the leading cause of hospitalization of sickle cell subjects. The data obtained, which reveal relevant markers of oxidative stress during VOC, could promote the implementation of new antioxidant therapeutic approaches and help improving sickle cell patients care
Raphael, Mariana Lopes Teixeira. "Estudo da imunogenicidade da proteína de classe 3 (PorB) purificada da membrana externa de Neisseria miningitidis: imunização intranasal/intramuscular em camundongos adultos e neonatos utilizando Bordetella pertussis como adjuvante." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-13012009-172350/.
Повний текст джерелаProteins of class 3 sound candidates in the preparation of vaccine against meningococcal illness. The aim of this study was to determine the immunogenicity of class 3 proteins purified of Neisseria meningitidis of the serogroup B along with whole cells of Bordetella pertussis as adjuvant. BALB/c and outbred neonate mice between 3 and 12 days old were immunized with 1 to 4 doses of the purified class 3 proteins with or without adjuvant given by the intranasal route, and on the 21st day the animals received an intramuscular dose of the class 3 proteins with or without aluminum hydroxide. The results demonstrated that after 2 doses by the intranasal route and 1 dose intramuscular there was a rapid stimulation of the immune cells in BALB/c adult mice as well as BALB/c and outbred neonates mice. All sera were analyzed by ELISA and immunoblot. The adjuvant B. pertussis used in the present investigation and given via the intranasal or intramuscular route increased the immune response compared with the controls. High affinity and bactericidal antibodies were produced.
Correia, Patrícia Maria Dias. "Identification and characterization of potential therapeutic targets for spinal cord repair." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22055.
Повний текст джерелаTraumatic spinal cord injury (SCI) is a devastating event that leads to loss of neurological functions below the vertebral level of the lesion. As adult neurons from central nervous system (CNS) fail to regenerate when injured, the consequences of SCI are partially or totally irreversible. The lack of regeneration ability of CNS neurons has been studied for years but still no effective treatment was found for this pathology; only steroids are validated and recognized as a pharmacologic treatment attempt, but just limit the lesion extent. This work focused on finding putative candidate genes involved in regeneration that could be targeted for therapy. A bioinformatics analysis based on studies with rodent SCI models, where a regenerative treatment attempt was applied and functional recovery was observed, was performed and some common regulated genes were found in the analysed studies. KIF4A and MPP3 genes were highlighted for further experimental studies in a regenerative model: a rodent model of peripheral nervous system (PNS) injury, with crush or transection of the sciatic nerve. Our results demonstrated that KIF4A and MPP3 are expressed and regulated in the lesioned sciatic nerve and in the corresponding dorsal root ganglia (DRG). Moreover, these genes also showed protein distribution in spinal cord tissue sections, in sciatic nerve and in DRG cuts, revealing that they are neuronal specific. These results represent important remarks to instigate further studies regarding the role of these genes in regenerative processes of lesioned neuronal tissues and the possibility of becoming important therapeutic targets in spinal cord injuries or related pathologies affecting the spinal cord integrity
A lesão traumática da medula espinal é um evento devastador que leva à perda de funções neurológicas abaixo do nível vertebral da lesão. Devido à falta de capacidade regenerativa dos neurónios adultos do sistema nervoso central, quando lesionados, as consequências das lesões são parcial ou totalmente irreversíveis. A falta de capacidade de regeneração dos neurónios do SNC tem sido estudada há anos, mas ainda não foi encontrado um tratamento efetivo para esta patologia; apenas os esteroides são validados e reconhecidos como um tratamento farmacológico, mas só limitam a extensão da lesão. Este trabalho centrou-se na procura de genes hipoteticamente envolvidos em regeneração do sistema nervoso, que possam ser candidatos a alvos de terapia para lesões na medula. Foi realizada uma análise bioinformática baseada em estudos com modelos de roedores com lesão da medula espinal, onde uma tentativa de tratamento regenerativo foi aplicada e observou-se recuperação funcional, e foram levantados os genes regulados comuns aos três estudos. Os genes KIF4A e MPP3 foram destacados para estudos experimentais adicionais num modelo regenerativo: um modelo de roedor, de lesão do sistema nervoso periférico, com esmagamento ou corte do nervo ciático. Os resultados demonstraram que os genes KIF4A e MPP3 são expressos e regulados no nervo ciático lesionado e nos gânglios da raiz dorsal correspondentes. Além disso, estes genes também mostraram distribuição proteica em secções de tecido de medula espinhal, de nervo ciático e em cortes de DRG, desvendando que possam ser específicos de tecido neuronal. Estes resultados representam observações importantes para instigar estudos adicionais sobre o papel destes genes nos processos regenerativos de tecidos neuronais lesionados e a possibilidade de se tornarem alvos terapêuticos importantes para lesões ou patologias relacionadas que afetem a integridade da medula espinal.
Vallet, Lara Dominique. "The Role of Erythrocyte Membrane Proteins in Haemolytic Anaemias in South African Populations." Thesis, 2006. http://hdl.handle.net/10539/1794.
Повний текст джерелаThe erythrocyte carries gases between the cells and the lungs, and has to distort to negotiate narrow splenic sinuses and capillaries. This distortion necessitates a high surface area to volume ratio that is maintained by the erythrocyte membrane skeleton, a network of proteins including spectrin and protein 4.1. The skeleton anchors the lipid bilayer through attachment to integral membrane proteins, notably the anion exchange protein, band 3. Abnormalities of the erythrocyte membrane proteins cause loss of cell elasticity and ultimately the erythrocytes become prematurely trapped in the spleen where they are phagocytosed, resulting in haemolytic anaemia. Three mutations causing band 3-deficient hereditary spherocytosis (HS), a haemolytic anaemia characterised by spherical erythrocytes, were located using restriction enzyme analysis and DNA sequencing. Proband A (Black) is heterozygous for band 3 Pinhal (R490H) and has mild clinical symptoms. Proband B and his mother (Caucasian) are heterozygous for band 3 Bicetre (R490C) and have severe anaemia requiring transfusions and splenectomy, respectively. These results confirm codon 490 as a hotspot for mutations and indicate the effect of different amino acid substitutions in the same position on clinical severity. Proband C (Black) is homozygous for a novel mutation (E508K) for which her parents are heterozygous. The proband is severely affected and transfusion- dependent whereas her father has moderate anaemia and her mother is asymptomatic. It is speculated that a secondary factor modulates their clinical symptoms. All of these mutations occur in a CpG dinucleotide, a common source of DNA mutations, and are located within the highly conserved exon 13, which encodes the third to fifth α-helices and the second extracellular loop of the transmembrane region of band 3. The mutations are likely to alter the conformation of band 3, impairing its insertion into the erythrocyte membrane. No causative mutations were located in another 12 band 3-deficient HS kindred using restriction enzymes and single strand conformation polymorphism analysis. Ten protein 4.1-deficient patients with hereditary elliptocytosis, a haemolytic anaemia characterised by elliptical erythrocytes, were also studied. Immunoblot analyses ruled out abnormally sized protein 4.1 and three known DNA mutations were excluded using restriction enzyme analysis. Further studies are required to elucidate the cause of the haemolytic anaemia in these kindred. This study advanced our knowledge of the molecular basis of HS in South African kindred and highlighted the susceptibility of CpG dinucleotides to mutations.
Vogelaar, Nancy Swick. "Structural and mechanistic motifs in membrane proteins: the three-dimensional modelling of rhodopsin, band 3, and the nicotinic acetylcholine receptor." Thesis, 1989. https://thesis.library.caltech.edu/7948/1/Vogelaar%201989.pdf.
Повний текст джерелаBecause so little is known about the structure of membrane proteins, an attempt has been made in this work to develop techniques by which to model them in three dimensions. The procedures devised rely heavily upon the availability of several sequences of a given protein. The modelling procedure is composed of two parts. The first identifies transmembrane regions within the protein sequence on the basis of hydrophobicity, β-turn potential, and the presence of certain amino acid types, specifically, proline and basic residues. The second part of the procedure arranges these transmembrane helices within the bilayer based upon the evolutionary conservation of their residues. Conserved residues are oriented toward other helices and variable residues are positioned to face the surrounding lipids. Available structural information concerning the protein's helical arrangement, including the lengths of interhelical loops, is also taken into account. Rhodopsin, band 3, and the nicotinic acetylcholine receptor have all been modelled using this methodology, and mechanisms of action could be proposed based upon the resulting structures.
Specific residues in the rhodopsin and iodopsin sequences were identified, which may regulate the proteins' wavelength selectivities. A hinge-like motion of helices M3, M4, and M5 with respect to the rest of the protein was proposed to result in the activation of transducin, the G-protein associated with rhodopsin. A similar mechanism is also proposed for signal transduction by the muscarinic acetylcholine and β-adrenergic receptors.
The nicotinic acetylcholine receptor was modelled with four trans-membrane helices per subunit and with the five homologous M2 helices forming the cation channel. Putative channel-lining residues were identified and a mechanism of channel-opening based upon the concerted, tangential rotation of the M2 helices was proposed.
Band 3, the anion exchange protein found in the erythrocyte membrane, was modelled with 14 transmembrane helices. In general the pathway of anion transport can be viewed as a channel composed of six helices that contains a single hydrophobic restriction. This hydrophobic region will not allow the passage of charged species, unless they are part of an ion-pair. An arginine residue located near this restriction is proposed to be responsible for anion transport. When ion-paired with a transportable anion it rotates across the barrier and releases the anion on the other side of the membrane. A similar process returns it to its original position. This proposed mechanism, based on the three-dimensional model, can account for the passive, electroneutral, anion exchange observed for band 3. Dianions can be transported through a similar mechanism with the additional participation of a histidine residue. Both residues are located on M10.
Tang, Meng-Ju, and 湯孟儒. "Role of Epithelial Membrane Protein 3 inHuman Hepatocellular Carcinoma Cells." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/87941803841473005612.
Повний текст джерела中山醫學大學
生化暨生物科技研究所
101
The epithelial membrane proteins-3 (EMP-3) comprise a subfamily of small hydrophobic membrane proteins. The putative four-transmembrane domain structure as well as the genomic structure is highly conserved among family members. EMP3 were mapped to chromosomes 19q13.3. EMP3 is expressed in many tissues, and functions in cell growth, differentiation, invasion and apoptosis have been reported. However, its involvement in human hepatocellular carcinoma (HCC) progression remains unclear. In our study, we found that EMP3 protein expression is higher in poor differentiated HA22T/VGH and SK-Hep-1 cells than in moderate and well differentiated Huh-7 and HepG2 cells, and HCC cancer tissue correlated significantly with tumor differentiation (P < 0.02). To verify the biological function of EMP3 in HCC cells, we found that Lentivirus-mediated EMP3 interference inhibited growth as assessed by the MTT assay. Likewise, inhibition of EMP3 expression induced cell-cycle arrest in SK-Hep-1 and Huh-7 cells by up-regulating the expression of p21Cip1 and p27Kip1, down-regulating the expression of Cyclin D1、Cyclin E and Skp2 protein expressions. Knockdown of EMP3 decreased migration and invasion in SK-Hep-1 and Huh-7 cells, and down-regulation of MMP9 and uPA. We examined the effect of down-regulation of EMP3 on the activation of ERK1/2 and Akt signaling. Western blot analysis showed that the expression of phosphorylated Akt was significantly decreased in EMP3 knockdown cells. Moreover, overexpression of Akt abolished EMP3-mediated cell migration and invasion. Conversely, inhibition of Akt phosphorylation remarkably reduced the migration and invasion of HCC cells with decreased expression of EMP3. We also found that EMP3 interacted with p85 (regulatory subunit of phosphoinositide 3-kinase [PI3K]) by immunoprecipitation and immunofluorescence assay. Conversely, inhibition of endogenous EMP3 by shRNA significantly reduced the interaction of p85 in SK-Hep-1 cells. In agreement with these findings, Moreover, EMP3 expression positively correlates with p85 (R=0.3851, P <0.01)、p-Akt (R=0.3789, P< 0.01)、MMP9 (R=0.3697, P < 0.02) and uPA (R=0.4986, P < 0.001) in tumor tissues from patients with HCC. From literature showed that the constitutive overexpression of EMP3 in HEK-293 cells led to cell blebbing and cell death, therefore, we found that P2X7R protein expression is higher in poor differentiated HA22T/VGH and SK-Hep-1 cells than in moderate and well differentiated Huh-7 and HepG2 cells. In addition, immunoprecipitation and immunofluorescence analysis revealed that EMP3 associated with P2X7R. Conversely, EMP3 depletion reduced the P2X7 expression. Collectively, our results show that overexpression of EMP3 promotes human HCC progression by enhancing cell proliferation and invasiveness. Therefore, EMP3 is a master regulator of human HCC growth and might be a useful molecular target for HCC prognosis and treatment.
Etzkorn, Manuel. "Protein precipitates, aggregation kinetics and membrane protein receptors characterized by solid-state NMR." Doctoral thesis, 2008. http://hdl.handle.net/11858/00-1735-0000-0006-B647-3.
Повний текст джерелаBrizida, Carolina Almeida Lavado. "Interaction between a Chlamydia trachomatis inclusion membrane protein (Inc) and host cell 14-3-3 proteins." Master's thesis, 2020. http://hdl.handle.net/10362/113711.
Повний текст джерелаAoh, Quyen Le. "Regulation of epidermal growth factor receptor trafficking by secretory carrier membrane protein 3." 2009. http://proquest.umi.com/pqdweb?did=1801419091&sid=2&Fmt=2&clientId=3507&RQT=309&VName=PQD.
Повний текст джерелаJames, Christina. "Analysis of the Interactome and Membrane Insertion of VAPB, a Tail- Anchored Protein at the Inner Nuclear Membrane." Doctoral thesis, 2020. http://hdl.handle.net/21.11130/00-1735-0000-0005-13F3-3.
Повний текст джерелаChang, Shu-Hui, and 張淑慧. "Molecular mechanism of EBV latent membrane protein-1 induced inhibition of tissue inhibitor of metalloproteinase-3." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/86392507708066462674.
Повний текст джерела高雄醫學大學
公共衛生學研究所碩士班
94
Epstein-Barr virus is a prototype gamma herpes virus which is widely spreaded infection in the adults. EBV has been implicated in the pathogenesis of several human malignancies such as Burkitt’s lymphoma, Hodgkin’s disease and nasopharyngeal carcinoma (NPC). Latent membrane protein 1 (LMP-1) is the oncoprotein of EBV associated NPC. Some evidences showed that LMP-1 enhanced the MMP-9 expression in the EBV-infected human epithelial cell lines C33A. In addition, numerous studies indicated that many NPC patients have lymph-node metastasis. In the physical condition, MMPs are regulated by natural inhibitor called tissue inhibitor of metalloproteinases (TIMPs). Until now, there are four kinds of TIMPs: TIMP-1, TIMP-2, TIMP-3 and TIMP-4. The biological function of TIMP-3 is different from the others. First, it could inhibit ADAM-17 (a disintergrin and metaloproteinases) , ADAMT-4 and ADAMT-5 (ADAM with thrombospondin domain). TIMP-3 could inhibit TNF-α release from the cells and regulate cellular inflammation. Second, TIMP-3 could promote cancer cells to undergo apoptosis. Third, TIMP-3 could inhibit the metastasis and angiogenesis of cancer cells. Fourth, TIMP-3 played a key role in the inhibition of tumor growth. Some evidences showed that the TIMP-3 promoter was hypermethylated in the tumor, and its expression was significantly down-regulated in tumors.The goal of our study is to elucidate the molecular mechanism by which LMP-1 regulates TIMP-3 in the NPC cell line TW04. Our results showed that TIMP-3 was decreased in LMP-1-expressing TW04 cells. Promoter activity assays indicated that the -44 / +28 region of TIMP-3 promoter was regulated by LMP-1. By using different kinds of protein kinase inhibitors, it was showed that the TIMP-3 mRNA level was restored after treatment with p38 kinase inhibitor SB203580. We found that the LMP-1 induced TIMP-3 inhibition could increase the migration and invasion of TW04 cells. While co-expression with TIMP-3 attenuated LMP-1-evoked the migration and invasion. According to our results, we suggest that LMP-1 might increase the cell migration and invasion through p38 mediated down-regulation of TIMP-3.
Wu, Shih-Jung, and 鄔式絨. "Outer membrane protein, OprI/OprF, modulates the susceptibility of Pseudomonas aeruginosa to cationic peptide, (R3S1)3." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/40169852136839280541.
Повний текст джерела國立臺灣大學
微生物學研究所
96
Short cationic antimicrobial peptides are widely present in living organisms for innate defense against invading microorganisms. They are generally amphipathic, small and cationic with at least two positive residues. We demonstrated a synthetic cationic peptide, (R3S1)3, possessing antimicrobial activity, especially against Pseudomonas aeruginosa. Our results showed that the outer membrane proteins of P. aeruginosa, OprI and OprF, interact with the peptide. The antimicrobial activity of (R3S1)3 were repressed by excess amounts of rOprI, rOprF, anti-OprI or anti-OprF. The bacterial membrane became permeable, the chromatin condensed in cytosol and blebs formed on outer membrane of bacteria after (R3S1)3 treatment analyzed by TEM. In addition, the (R3S1)3 translocated across the cytoplasmic membrane, localized in the cytosol of P. aeruginosa and bound to intracellular target, like nucleic acids, analyzed by immunohistochemistry. The (R3S1)3 exerted not only antimicrobial activity but also penetrated eukaryotic cell and nuclear membranes. These action mechanism of antimicrobial peptide (R3S1)3 against P. aeruginosa through the bacterial outer membrane proteins, OprI/OprF, provide important clues for development of new antimicrobial agents.