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BESTETTI, STEFANO. "AQP8, a redoxtat controlling tyrosine kinase signalling." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/170789.
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AQP8-mediated H2O2 transport allows efficient amplification of tyrosine kinase signalling, therefore influencing pathways frequently dysregulated under tumour progression. Besides, control of H2O2 cell permeability impacts life-death cell decisions in response to stress. Despite the important consequences of AQP8 gating, the precise biochemical modification that inhibits H2O2 transport still remains to be identified. We show here that the mechanism of regulation implies sulphydration of AQP8. Addition of an exogenous H2S donor (NaHS) is sufficient to block H2O2 entry and dampen EGF receptor signalling, bypassing stress. Moreover, cells expressing non-inhibitable AQP8 mutant (e.g. C53S) are able to transport H2O2 also upon H2S treatment. Stress-induced blockade of transport requires cystathionine-beta-synthase, a key enzyme in the transulphuration pathway. These findings identify a novel circuit modulating the strength and duration of key signalling pathways based on AQP8 regulation by sulphydration.AQP8-mediated H2O2 transport allows efficient amplification of tyrosine kinase signalling, therefore influencing pathways frequently dysregulated under tumour progression. Besides, control of H2O2 cell permeability impacts life-death cell decisions in response to stress. Despite the important consequences of AQP8 gating, the precise biochemical modification that inhibits H2O2 transport still remains to be identified. We show here that the mechanism of regulation implies sulphydration of AQP8. Addition of an exogenous H2S donor (NaHS) is sufficient to block H2O2 entry and dampen EGF receptor signalling, bypassing stress. Moreover, cells expressing non-inhibitable AQP8 mutant (e.g. C53S) are able to transport H2O2 also upon H2S treatment. Stress-induced blockade of transport requires cystathionine-beta-synthase, a key enzyme in the transulphuration pathway. These findings identify a novel circuit modulating the strength and duration of key signalling pathways based on AQP8 regulation by sulphydration.
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Felemban, Dalal Nouruldeen. "The Effects of Cold and Freezing Temperatures on The Blood Brain Barrier and Aquaporin 1, 4, and 9 Expression in Cope's Gray Treefrog (Hyla Chrysoscelis)." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1484650973702078.
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Stávale, Leila Miguel 1985. "Envolvimento da AQP4 no envenenamento por Phoneutria nigriventer = Involvement of AQP4 in Phoneutria nigriventer envenoming." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317745.
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Orientador: Maria Alice da Cruz HöflingDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-23T19:45:28Z (GMT). No. of bitstreams: 1 Stavale_LeilaMiguel_M.pdf: 25008584 bytes, checksum: 8754f8fc3865217986eb0137679176e9 (MD5) Previous issue date: 2013
Resumo: O veneno da aranha Phoneutria nigriventer (PNV), também conhecida como aranha armadeira, é uma mistura complexa de peptídeos com ação neurotóxica em alguns canais iônicos. No sistema nervoso central (SNC) alguns peptídeos do PNV causam permeabilização da barreira hematoencefálica (BHE) e interferem na liberação de neurotransmissores. A BHE, embora essencial para a manutenção da homeostase do SNC, pode representar uma barreira muito restritiva para o acesso de drogas terapêuticas ao microambiente neural. O entendimento dos mecanismos associados à disfunção da BHE é relevante do ponto de vista científico e médico. O objetivo do estudo foi investigar alguns mecanismos envolvidos na neurotoxicidade do veneno da Phoneutria nigriventer em ratos Wistar (Rattus norvegicus). Para esse fim, o efeito vasogênico causado pela neurotoxicidade do veneno no cérebro, foi examinado através da avaliação da expressão de aquaporina 4 (AQP4), uma proteína formadora dos canais de água e abundantemente localizada nos pés astrocitários perivasculares e relacionada com o aparecimento de edema no cérebro. A análise da expressão da proteína foi feita por imunohistoquímica e western blotting e a expressão de RNAm por PCR em tempo real no cerebelo e hipocampo de animais neonatos (14 dias) e adultos (8 semanas). Os resultados obtidos mostraram aumento da expressão de AQP4 e seu RNAm nos animais envenenados, que entretanto foi variável em função do tempo de envenenamento (2, 5 ou 24 h), da região do cerebelo ou hipocampo examinada e da idade dos animais. Os resultados mostraram também intensa marcação anti-AQP4 ao redor de vasos com edema perivascular ou não, como também entre os corpos neuronais e seus prolongamentos. Concluímos que a AQP4 tem papel nas alterações de volume dos astrócitos perivasculares e na formação e resolução do edema ao redor da BHE causado pelo PNV. A dinâmica da expressão da AQP4 no cerebelo e hipocampo em função do tempo, região e idade dos animais sugere a existência de fatores intrínsicos que modulam diferencialmente a funcionalidade da BHE em função do microambiente local. A compreensão dos mecanismos envolvidos no envenenamento por PNV pode contribuir para o desenvolvimento de ferramentas úteis para a intervenção clínica, bem como pode ser relevante para o entendimento dos mecanismos relacionados ao funcionamento da BHE e de proteínas envolvidas na formação de canais de água, como a AQP4
Abstract: The Phoneutria nigriventer spider venom (PNV), also known as armed-spider, is a complex mixture of ion channels-acting peptides which exhibit neurotoxic action. In the central nervous system (CNS), PNV-containing peptides cause permeabilization of the blood-brain barrier (BBB) and interfere with neurotransmitter release. The BBB, although essential for the maintenance of homeostasis of the CNS, may represent a very restrictive barrier for the access of therapeutic drugs into the neural microenvironment. The understanding of BBB impairment-associated mechanisms are of scientific and medical importance. The aim of this study was to investigate some of the mechanisms involved in the neurotoxicity caused by Phoneutria nigriventer venom in Wistar rats (Rattus norvegicus). To this end, the vasogenic effect caused by the venom neurotoxicity in the brain was examined by evaluating the expression of aquaporin 4 (AQP4), a water channel forming protein abundantly expressed in perivascular astrocytic endfeet processes and associated to the formation and resolution of edema in the brain. The analysis of AQP4 expression was assessed in the cerebellum and hippocampus of neonate (14 day-old) and adult rats (8 week-old) through immunohistochemistry and western blotting, and the expression of mRNA by Real Time-PCR. The results showed increases of AQP4 expression and its mRNA in the envenomed animals, which though showed time- (2, 5 or 24h), regional- (regions of the cerebellum and hippocampus examined) and age-associated differences. Marked anti-AQP4 labeling was found around vessels with or without edema and among the neuron bodies and their processes. We conclude that AQP4 has a role in the volume alterations of the perivascular astrocytes and in the formation and resolution of edema around the BBB induced by PNV. The variability of the dynamics of AQP4 expression in the cerebellum and hippocampus in function of the time, region and animals age suggests the existence of intrinsic factors that modulate the BBB functionality depending on the molecular biology dynamics of the local microenvironment. The understanding of the mechanisms involved in the envenomation by PNV can contribute to the development of useful tools for clinical intervention, and may be relevant for understanding the mechanisms related to the functioning of the BBB and proteins involved in the formation of water channels, such as AQP4
Mestrado
Histologia
Mestra em Biologia Celular e Estrutural
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Sharma, Mansi. "Regulatory mechanisms of Leishmania Aquaglyceroporin AQP1." FIU Digital Commons, 2015. http://digitalcommons.fiu.edu/etd/2300.
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Pentavalent antimonials [Sb(V)] are the primary drug of choice against all forms of leishmaniasis. Emergence of antimony unresponsiveness is a major issue. There is a dire need of understanding antimony resistance mechanisms in Leishmania. One important mechanism is the down regulation of the trivalent antimony [Sb(III)] (the active form of Sb(V)) uptake system. To date, Leishmania aquaglyceroporin AQP1 is the only reported facilitator of Sb(III). Leishmania do not have promoters. They primarily regulate their genes at post-transcriptional and/or post-translational levels. We reported that mitogen activated protein kinase 2 (MPK2) positively regulated AQP1 stability through the phosphorylation of the threonine 197 (T197) residue of AQP1. The goal of this study was to elucidate the regulatory mechanism(s) of AQP1 in Leishmania in order to advance our understanding about the physiological role(s) of AQP1 in Leishmania biology. When Leishmania promastigotes were treated with the proteasome inhibitor MG132, SbIII accumulation was increased due to upregulation of AQP1. Alteration of lysine 12 of AQP1 to either alanine or arginine improved protein stability. Cells co-expressing a dominant-negative MPK2 mutant exhibited severely reduced AQP1 expression, which was reversed upon addition of MG132. Interestingly, the dominant-negative MPK2 mutant could not destabilize either AQP1K12A /AQP1K12R. Stabilization of AQP1 by MPK2 led to its relocalization from the flagellum to the entire surface of the parasite. Both altered AQP1K12A and AQP1K12R were restricted to the flagellum only. The data demonstrated that lysine12 was targeted for AQP1 proteasomal degradation playing an integral role in subcellular localization of AQP1 as well as its interaction with MPK2.
This study also demonstrated that the stability of AQP1 mRNA in different Leishmania species was regulated by their respective 3’-untranslated regions. Cutaneous leishmaniasis causing species accumulated more antimonite and therefore, exhibited higher sensitivity to antimonials than species responsible for visceral leishmaniasis. This species-specific differential sensitivity to antimonite was found to be directly proportional to the expression levels of AQP1 mRNA. The differential regulation of AQP1 mRNA explained the distinct antimonial sensitivity of each species. This study will help us to identify new drugs for treatment in the future and also lead to a novel understanding of parasite biology aspects such as integral membrane protein trafficking and regulation.
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Arif, Muhammad. "The role of aquaporin 3 (AQP3) in breast cancer." Thesis, Aston University, 2014. http://publications.aston.ac.uk/23183/.
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The increasing prevalence of breast cancer (BC) in different parts of the world, particularly in the UK, highlights the importance of research into the aetiology and pathology of the disease. BC is the most common malignancy affecting women worldwide. Aquaporins (AQPs) are membrane protein channels that regulate cellular water flow. Recently, studies have demonstrated that expression of AQP3 is up-regulated in cancerous breast tissue. The present study examines the role of AQP3 in BC cell biology. Examination of clinical cases of BC showed higher AQP3 gene and protein expression in cancer tissues compared to healthy border tissues. In distinct clinicopathological groups however there were no differences observed with regards to AQP3 expression, suggesting that AQP3 expression may not be a predictor of lymph node infiltration or tumour grade. shRNA technology was used to knockdown gene expression of AQP3 in the invasive MDA-MB-231 BC cellular model. Cellular proliferation, migration, invasion, adhesion and response to the 5- fluorouracil (5-FU) based chemotherapy treatment were investigated in parental and knockdown cell line. AQP3 knockdown cells showed reduction in cellular proliferation, migration, invasion and increase in cell sensitivity to 5-FU compared with wild type (WT) or scrambled control (SC) cells. The effects of AQP3 knockdown on cellular glycolytic ability and ATP cellular content were quantified. Indirect glucose uptake was also measured by quantifying reconditioned media. AQP3 knockdown cells showed significantly lower levels of glucose uptake as compared to WT or SC. However there was no difference in the glycolytic ability and ATP content of the cells suggesting AQP3 has no role in cancer cell energetics. These data collectively suggest AQP3 expression is associated with the BC disease clinically and plays a role in multiple important aspects of BC pathophysiology, thus AQP3 represents a novel target for therapeutic intervention.
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Dahlke, Agnes Maria [Verfasser], Michael [Gutachter] Adamzik, and Andrea [Gutachter] Tannapfel. "Methylierungsanalyse des AQP5-Promotors bei Septikern und Kontrollpatienten in Abhängigkeit vom AQP5 A (-1364) C Promotorpolymorphismus / Agnes Dahlke ; Gutachter: Michael Adamzik, Andrea Tannapfel." Bochum : Ruhr-Universität Bochum, 2017. http://d-nb.info/1129452484/34.
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Dahlke, Agnes [Verfasser], Michael [Gutachter] Adamzik, and Andrea [Gutachter] Tannapfel. "Methylierungsanalyse des AQP5-Promotors bei Septikern und Kontrollpatienten in Abhängigkeit vom AQP5 A (-1364) C Promotorpolymorphismus / Agnes Dahlke ; Gutachter: Michael Adamzik, Andrea Tannapfel." Bochum : Ruhr-Universität Bochum, 2017. http://d-nb.info/1129452484/34.
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Siordia, Juan Arturo. "V2 Receptor and AQP2 Distribution in the Kangaroo Rat Kidney." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/144945.
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Roudier, Nathalie. "Caractérisation Structurale et Fonctionnelle de l'Aquaglycéroporine AQP3 exprimée dans divers Systèmes." Phd thesis, Université Paris Sud - Paris XI, 2000. http://tel.archives-ouvertes.fr/tel-00004048.
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La famille des protéines MIPs est composée de canaux hydriques et de facilitateurs de glycérol. Parmi les canaux hydriques, certains sont sélectivement perm&ables à l'eau, les aquaporines (AQP1, AQP2,...), et les autres sont également perméables aux petits solutés comme le glycérol: les aquaglycéroporines, dont AQP3 fait partie. Nous avons montré dans un premier temps que la perméabilité au glycérol du globule rouge était due à la présence d'AQP3. Dans l'intention de mieux connaître quels étaient les éléments protéiques impliqués dans la sélectivité des protéines MIPs, nous avons construit des chimères entre AQP2 et AQP3. L'une d'entre elle, AQP3-AQP2 Cter, après expression dans l'ovocyte de Xénope, a permis de montrer que la partie C terminale cytoplasmique est impliquée dans le transport d'eau mais pas dans le transport de glycérol d'AQP3. Nous avons également montré que les ovocytes de xénope non matures possédaient des perméabilités à l'eau et au glycérol supérieurs à celles des ovocytes matures suggérant l'expression d'un canal ou d'un transporteur endogène. Enfin, nous avons envisagé de déterminer pour la première fois la structure quaternaire d'une aquaglycéroporine: AQP3. Alors qu'AQP1 dévoile sa forme tétramérique sur gradient de saccharose, après solubilisation en conditions non dénaturantes, AQP3 sédimente dans des fractions plus légères sous forme d'un monomère et d'un dimère très résistant au SDS et aux agents réducteurs hydrophiles. Nous n'avons pu conclure quant à son organisation dans les membranes du fait de son éventuelle sensibilité spécifique aux détergents non dénaturants utilisés. Nous avons donc engagé des études de microscopie électronique de cryofractures de membranes d'ovocytes exprimant AQP1 et AQP3. Nous en avons déduit que la taille d'AQP3 n'était pas suffisamment différente de celle d'AQP1 pour suggérer une organisation membranaire également différente.
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Yang, Ming-Hui. "A water channel (AQP9) in retinal ganglion cell apoptosis and glaucoma." Fort Worth, Tex. : Texas Christian University, 2007. http://etd.tcu.edu/etdfiles/available/etd-04202007-153701/unrestricted/yang.pdf.
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ROUDIER, NATHALIE. "Caracterisation structurale et fonctionnelle de l'aquaglyceroporine aqp3 exprimee dans divers systemes." Paris 11, 2000. http://www.theses.fr/2000PA112013.
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La famille des proteines mips est composee de canaux hydriques et de facilitateurs de glycerol. Parmi les canaux hydriques, certains sont selectivement permeables a l'eau, les aquaporines (aqp1, aqp2,), et les autres sont egalement permeables aux petits solutes comme le glycerol, les aquaglyceroporines, dont aqp3 fait partie. Nous avons montre dans un premier temps que la permeabilite au glycerol du globule rouge etait due a la presence d'aqp3. Dans l'intention de mieux comprendre quels etaient les elements proteiques impliques dans la selectivite des proteines mips, nous avons construit des chimeres entre aqp2 et aqp3. L'une d'entre elle, aqp3-aqp2 cter, apres expression dans l'ovocyte de xenope, a permis de montrer que la partie cterminale est impliquee dans le transport d'eau mais pas dans le transport de glycerol des proteines mips. Nous avons egalement montre que les ovocytes de xenope non matures possedaient des permeabilites a l'eau et au glycerol superieures a celles d'ovocytes matures. Ceci est du a l'expression d'un canal ou d'un transporteur endogene. Enfin, nous avons envisage de determiner pour la premiere fois la structure quaternaire d'une aquaglyceroporine : aqp3. Alors qu'aqp1 devoile sa forme tetramerique sur gradient de saccharose, apres solubilisation en conditions non denaturantes, aqp3 sedimente dans des fractions plus legeres sous formes d'un monomere et d'un dimere tres resistant au sds et aux agents reducteurs hydrophiles. Nous n'avons pu conclure quant a son organisation dans les membranes du fait de son eventuelle sensibilite specifique aux detergents non denaturants utilises. Nous avons donc engage des etudes de microscopie electronique de cryofractures de membranes d'ovocytes exprimant aqp1 et aqp3. Nous en avons deduit que la taille d'aqp3 n'etait pas suffisamment differente de celle d'aqp1, pour suggerer une organisation membranaire similaire.
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Berninger, Lucija [Verfasser]. "Funktion von DNER und AQP1 in der Pathogenese der Osteoarthrose / Lucija Berninger." Gießen : Universitätsbibliothek, 2016. http://d-nb.info/1108053327/34.
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Segura, Anaya Edith, and Dent Myrna Alexandra Roberta. "Localizacion de la Acuaporina (AQP1) en el Nervio Ciatico de la Rata." Tesis de Licenciatura, Medicina-Quimica, 2013. http://hdl.handle.net/20.500.11799/14424.
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Leung, Sau-kit. "The role of aquaporin 9 (AQP9) in arsenic trioxide sensitivity of human Leukaemia." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B35538375.
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Leung, Sau-kit, and 梁秀傑. "The role of aquaporin 9 (AQP9) in arsenic trioxide sensitivity of human Leukaemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B35538375.
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Chan, Ka-man, and 陳嘉雯. "Detection of anti-aquaporin (AQP4) autoantibodies in the diagnosis of neuromyelitis optica (NMO)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44659192.
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Montasser, Karim [Verfasser]. "AQP4 im kaninen Gehirn : Etablierung einer Immunfluoreszenz und Beobachtungen zur Verteilung / Karim Montasser." Gießen : Universitätsbibliothek, 2017. http://d-nb.info/1147255490/34.
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Ñaupac, Pacco Verónica, Vargas Alejandra Gómez, Chávez Cesar Franz Puma, and Vera Paulo Cesar Jara. "Planeamiento estratégico de la Cooperativa de Ahorro y Crédito AQP." Master's thesis, Pontificia Universidad Católica del Perú, 2019. http://hdl.handle.net/20.500.12404/15978.
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Las Cooperativas de Ahorro y Crédito en el Perú se encuentran en un nuevo escenario
a partir del cambio en el modelo de supervisión donde ahora, a través de la Superintendencia
de Banca, Seguros y AFP (SBS), el Estado toma el liderazgo de un esquema especializado
que incluye facultades sancionadoras. El escenario podría no parecer alentador; sin embargo,
este desafío debe ser encarado por estas instituciones con el objetivo de fortalecerse
generando mayor confianza y aprovechando su potencial a nivel económico y social.
La cooperativa de ahorro y crédito AQP (en adelante denominada COOPAC AQP) es
una organización arequipeña con presencia también en Lima que atiende a más de 39,000
clientes, principalmente mujeres de los segmentos medio bajo y bajo, con una cartera de S/
52.1 MM a un índice de mora de 2.91%. En el 2018, con ratios financieros positivos, alcanzó
el puesto 31 en el ranking cooperativo peruano elaborado por FENACREP (Federación de
Cooperativas de Ahorro y Crédito). Este desempeño de COOPAC AQP en crecimiento y el
potencial a futuro es una situación que le exige revisar constantemente sus estrategias, motivo
por el cual el presente trabajo se propone un plan estratégico a cinco años que le permita
seguir creciendo de forma sostenida.
El presente plan estratégico de COOPAC AQP establece el desafío de la organización
a largo plazo a través de cuatro objetivos. En el 2023 se visiona alcanzar mayor participación
de mercado, mayor rentabilidad sobre el patrimonio, mayor rentabilidad sobre los activos,
crecimiento del EBITDA, mejora en la calificación institucional según su clasificación de
riesgos y bancarizar 8,000 mujeres de los segmentos económicos bajo y medio bajo. Estos
desafíos requieren la expansión de COOPAC AQP buscando al mismo tiempo mayor
productividad que se traduce en el mejor desempeño de su equipo humano y buen gobierno
corporativo, además del incremento del índice de participación de fondeo.The Savings and Credit Cooperatives in Peru are in a new scenario from the change in the supervision model where, now, through the Superintendence of Banking, Insurance and AFP (SBS), the State takes the lead of a scheme specialized that includes sanctioning powers. The scenario might not seem encouraging; however, these institutions with the aim of strengthening themselves, generating greater confidence and harnessing their potential at an economic and social level must face this challenge. The AQP savings and credit cooperative (hereinafter referred to as COOPAC AQP) is a Arequipa organization with a presence also in Lima that serves more than 39,000 clients, mainly women from the medium low and low segments, with a portfolio of S / 52.1 MM and default rate of 2.91%. In 2018, with positive financial ratios, it reached the 31st position in the Peruvian cooperative ranking prepared by FENACREP (Federation of Savings and Credit Cooperatives). This growing COOPAC AQP performance and future potential is a situation that requires you to constantly review your strategies, which is why this work proposes a five-year strategic plan that allows you to continue growing steadily. The present COOPAC AQP strategic plan establishes the challenge of the long-term organization through four objectives. In 2023, is expected to achieve greater market share, greater profitability on equity, greater profitability on assets, growth of EBITDA, improvement in institutional qualification according to its risk classification and 8,000 women in the low and medium low economic segments. These challenges require the expansion of COOPAC AQP while seeking greater productivity that translates into the best performance of its team and good corporate governance, in addition to the increase in the funding participation rate.
Tesis
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SAITO, Noboru, Hidehiro IKEGAMI, and Kiyoshi SHIMADA. "Effect of water deprivation on aquaporin 4 (AQP4) mRNA expression in chickens (Gallus domesticus)." Elsevier, 2005. http://hdl.handle.net/2237/9193.
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Trzeciak, Verena [Verfasser]. "Intestinale Kompensationsmechanismen in Mäusen mit einem AQP2-Promotor-abhängigen Knockout des Mineralokortikoidrezeptors / Verena Trzeciak." Kiel : Universitätsbibliothek Kiel, 2014. http://d-nb.info/1049437624/34.
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Monzani, E. "Knock down of AQP1 in HMEC-1 and WM115 cells changes the organization of the cytoskeleton." Doctoral thesis, Università degli Studi di Milano, 2009. http://hdl.handle.net/2434/140997.
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Aquaporins are a family of water membrane-channel proteins expressed in diverse tissues. Recently AQP1 has been proposed as a novel promoter of tumor angiogenesis. Herein, we focused in particular on AQP1 investigating its role in both (HMEC-1) and in a human melanoma cell line (WM115). AQP-1 knock down by RNAi, affects cell shape determining a rounded morphology in both cells and a re-organization of F-actin, reducing the migration and invasive capacity significantly, and impaired the ability to organize the pseudovascular networks. In order to better understand the intracellular mechanisms elicited by AQP-1, we have investigated the role of LIN7, a PDZ protein which is involved in the recruitment and plasma membrane localization of interacting transporters, receptors, and adhesion molecules, linking them, through beta-catenin, to the cytoskeleton. Our results showed for the first time that AQP-1 co-immunoprecipitated with LIN7, and that the knock down of AQP-1 decreased the level of expression of LIN7 and beta-catenin. Interestingly, the inhibition of proteasome contrasted partially such a decrease. All together, our findings show, for the first time, that AQP-1 triggers an intracellular mechanisms modulating and stabilizing the organization of cytoskeleton, through LIN-7/beta-catenin interaction. Hear, we presented a model of the intracellular mechanism trigger by AQP-1 to regulate these process. Finally, we attempt to speculate that the skeleton-linked AQP-1, feel the degree of membrane skeleton distension and can regulate the state of cell volume necessary for polarization, migration and tube formation.
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Faust, Doerte [Verfasser]. "Identification of proteins controlling AQP2 translocation by large-scale siRNA screening of the mouse kinome / Doerte Faust." Berlin : Freie Universität Berlin, 2014. http://d-nb.info/1054328897/34.
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Skowron-Zwarg, Marie. "Modulation de la différenciation mucociliaire des cellules épithéliales nasales humaines par l'interleukine-13 : caractérisation de cibles moléculaires." Paris 7, 2004. http://www.theses.fr/2004PA077169.
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Alaeddine, Savvas [Verfasser], Michael [Gutachter] Adamzik, and Thomas [Gutachter] Weber. "AQP2-752 A/G-Promotorpolymorphismus und der Krankheitsverlauf nach einer Nierentransplantation / Savvas Alaeddine ; Gutachter: Michael Adamzik, Thomas Weber." Bochum : Ruhr-Universität Bochum, 2017. http://d-nb.info/1129452190/34.
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Crum, Anthony Bryan. "Co-Localization Patterns of Aquaporin-4 with Amyloid Beta and CD68 in Alzheimer's Disease and Cerebrovascular Disease." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/7441.
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Aquaporin-4 (AQP4) is a key component in maintaining proper glymphatic flow. In recent years, the glymphatic system has been discovered and approached as a major factor in amyloid plaque clearance in Alzheimer's disease. This study examines the depolarization of AQP4 from the astrocytic endfeet and subsequent co-localization with amyloid plaques in the hippocampus and subiculum. Results show a significant pattern of co-localization in advanced Alzheimer's disease, as well as increases in AQP4 in cerebrovascular disease. This pattern shows AQP4 should be approached as a promising therapeutic area in future research.
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Sougrat, Rachid. "Expression et fonction de l'aquaporine-3 dans la peau humaine." Paris 7, 2003. http://www.theses.fr/2003PA077250.
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Matsui, Satoshi. "Differentiation and isolation of iPSC-derived remodeling ductal plate-like cells by use of an AQP1-GFP reporter human iPSC line." Kyoto University, 2019. http://hdl.handle.net/2433/242912.
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Bi, Chongshan. "The role of caveolin-1 phosphorylation in AQP4 membrane expression in a model of oxidative stress in primary astrocyte cultures." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/37065.
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Astrocytes play an important role in a wide variety of physiological processes and in
disease states such as ischemia. Ischemic damage in the brain involves apoptotic cell death of
neurons as well as astrocytes and it has been suggested that reactive oxygen species (ROS)
generated as a consequence of ischemia are a major factor in triggering cell death. The waterpermeable
channel, aquaporin 4 (AQP4), which is expressed at high concentrations in astrocytes,
is an important determinant of mortality and morbidity in mice subjected to ischemia, however
the effects of ROS on AQP4 expression and the underlying mechanisms are still obscure. In the
present study, we used primary astrocyte cultures to examine the expression of AQP4 under
oxidative stress using hydrogen peroxide. First, we showed that H₂O₂ induces a significant
increase of both AQP4 mRNA and protein levels and that this effect is inhibited by the antioxidant
N-acetylcysteine. Second, we demonstrated using cell surface biotinylation that H₂O₂
increases AQP4 plasma membrane expression independently of the newly synthesized pool of
AQP4. In parallel, we found that caveolin-1 undergoes a dose- and time-dependent
phosphorylation in astrocytes treated with H₂O₂ and that this effect is inhibited by the src kinase
inhibitor PP2. More importantly, PP2 inhibits the H₂O₂-induced increase in AQP4 cell surface
expression, suggesting that the phosphorylation of caveolin-1 and possibly other proteins may
play a role in this process. To investigate this further, we used MDA-435 cells expressing Y14F
and Y14D caveolin-1 mutants transfected with AQP4 and found that these cells exhibit a
decrease and an increase in AQP4 membrane expression, respectively. Furthermore, caveolin-1
knock down in astrocytes inhibits H₂O₂-induced increase in AQP4 cell surface expression.
Together these findings show that the phosphorylation of caveolin-1 Y14 is a key regulator of
AQP4 cell surface expression in oxidative stress possibly by altering AQP4 internalization and
trafficking resulting in its redistribution within different compartments of the cell.
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Tham, Daniel Kai Long. "ECM-receptor interactions regulate the distribution of Kir4.1 and AQP4 channels in renal tubules and at the blood-brain barrier." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44213.
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Osmostasis relies on the efficient and selective transport of molecules across barriers, often in a directional manner and this, in turn, is dependent on the asymmetric arrangement of channels within the cells comprising the organs that regulate these processes. The primary aim of this thesis is the identification of the extracellular matrix-receptor interactions important in the generation of polarized channel distribution in two such organs, the kidney and the blood-brain barrier. In the first study, we investigated the involvement of fibronectin and laminin in the basolateral localization of Kir4.1, an inwardly-rectifying potassium channel, and aquaporin-4 (AQP4), a water-permeable channel, in polarized Madin-Darby canine kidney (MDCK) cells. We determined using a variety of approaches that laminin-1 and fibronectin, when present in the culture substrate, significantly stablize both channel types at the basolateral surfaces of these cells and accordingly induce their increased expression within this membrane domain without requiring a concomitant upregulation of de novo channel synthesis. We also show that the coexpressed laminin receptor dystroglycan (DG) is important for cell surface expression of Kir4.1 but not AQP4, and demonstrate via the use of disintegrin peptides and function-blocking antibodies that their cell-surface expression and stability is also partly reliant on integrin receptors, with αvβ3 being particularly important in the case of the latter. In the second study, we examined the possibility that laminin-dystroglycan binding is involved in the regulation of AQP4 turnover in astrocytes. We first determined that laminin, when applied to primary astrocytes in culture, causes AQP4 amounts at the plasma membrane to increase in a DG-dependent manner while depleting the channel from intracellular sites, brought about by the suppression of channel endocytosis. We then showed that DG binds to inactive dynamin, and that the latter, when freed from this inhibitory influence, functions in cooperation with clathrin to mediate the rapid internalization of AQP4. Finally, we demonstrated that laminin selectively upregulates the cell-surface expression of the M23 isoform of AQP4 only. Our findings therefore reveal that, through their roles in establishing the microscopic architecture of these systems, the extracellular matrix and cell-surface receptors are critical determinants in osmoregulation
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Eckert, David. "The Prostaglandin E2 Receptor 1 (EP1) Antagonizes AngII in the Collecting Duct." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36196.
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Prostaglandin E2 (PGE2), a metabolite of arachidonic acid, plays a role in water and sodium reabsorption in the collecting duct of the kidney. The collecting duct is responsible for the fine tuning of water and electrolytes. Only a small fraction of the filtered water and sodium is reabsorbed in the collecting duct, a fraction crucial to the regulation of water and electrolyte balance. This current study addresses the role of EP1, one of four PGE2 receptors, in the collecting duct. It is well documented that PGE2 inhibits sodium and water reabsorption in the collecting duct, however the exact mechanism is still debated. To determine whether the EP1 receptor mitigates AngII renal effects, an in vivo study was performed with EP1-/- mice. Global EP1-/- knockout mice were crossed with a renin overexpressing mouse line (herein denoted as “Ren”) and subjected to a high salt (HS) and low salt (LS) diet. Ren mice displayed an 11mmHg increase in systolic blood pressure (BP) on a HS diet and a decrease in BP of 14mmHg on a LS diet compared to the normal salt (NS) diet. Ren EP1-/- mice did not display a significant increase or decrease in BP on a HS or LS diet. On a LS diet, Ren EP1-/- displayed a drop in urine osmolarity (1641 mOsm/ kgH2O) vs. wild type (WT) mice (2107 mOsm/ kgH2O), consistent with increased sodium reabsorption. Narrowing in on the collecting duct, Ren EP1-/- mice had enhanced αENaC levels compared to Ren mice. In ex vivo microperfusion experiments, EP1-/- tubules show no response to PGE2 in the presence of AVP, whereas PGE2 inhibits AVP induced water reabsorption in WT mice. An increase in αENaC membrane accumulation due to EP1 gene ablation results in increased sodium reabsorption subsequently leading to a rise in BP. This contributes to the lack of salt sensitivity in EP1-/- mice. Overall, the EP1 receptor in the collecting duct represents a potential therapeutic target for the treatment of hypertension.
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Robinson, Sergei Alexander. "AQUAPORIN 4 EXPRESSION AND DISTRIBUTION DURING OSMOTIC BRAIN EDEMA AND FOLLOWING CHRONIC TREATMENT OF DESIPRAMINE." Wright State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=wright1313150441.
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Rustige, Anna-Maria [Verfasser], Michael [Gutachter] Adamzik, and Stefan [Gutachter] Weiner. "Einfluss des Promotorpolymorphismus \(\textit AQP3-1431G}\)>A auf die Abstoßungsreaktion nach Nierentransplantation / Anna-Maria Rustige ; Gutachter: Michael Adamzik, Stefan Weiner ; Medizinische Fakultät." Bochum : Ruhr-Universität Bochum, 2019. http://d-nb.info/1187522570/34.
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Ferreira, Leonardo Eduardo. "Expressão de aquaporinas (AQPS 1 e 9) nos ductos eferentes e epidídimo de ratos Wistar com obesidade induzida induzida por dieta de cafeteria." Universidade Estadual do Oeste do Parana, 2013. http://tede.unioeste.br:8080/tede/handle/tede/634.
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Previous issue date: 2013-07-01The induction of obesity in experimental animals with cafeteria diet simulates the high-calorie food that humans eat, nowadays, thus enabling to study obesity and comorbidities resulting from this condition. The male reproductive system is directly affected by obesity with increased lipid peroxidation, increase of apoptotic bodies, changes in parameters espermatobioscópicos and reduced fertility. The aim of the study was to evaluate whether there are changes caused by obesity in epithelia of efferent ducts and epididymis , both in relation to morphology and expression of aquaporins 1 and 9 ( AQPs 1 and 9 ) in adult Wistar rats . After weaning , the animals were randomly divided into two groups : control group ( CON ) received standard diet and water ad libitum ( n = 10 ) and group cafeteria ( CAF ) , which received cafeteria diet soda and degassed ad libitum ( n = 10). The treatment group CAF began after the 12th week of life, totaling 40 weeks of consumption of cafeteria diet, being all dead animals with 52 weeks of age. The efferent ducts , along with initial segments ( Si ) , head ( Cç ) , body ( Co ) and tail ( Cd ) epididymis were submitted to routine histological and immunohistochemical staining for AQP- 1 and AQP- 9 . In the present study we evaluated the data: body mass, length nasoanal, waist circumference, Lee index and retroperitoneal fat mass and perigonadais; also evaluated dimensions, using morphometry and morphology of the epithelia of the efferent ducts and segments Si, Cç, Co and Cd epididymis and analyzed the expression of AQP- 9 and AQP- 1 in the efferent ducts and epididymal segments above. Changes in expression of AQPs in the efferent ducts and the epididymal epithelium were observed with increased expression of AQP- 1 and AQP- 9 reduction in efferent ducts and epididymal cauda, respectively, in animals treated with cafeteria diet. Also, there were morphological changes in the epididymal epithelium, such as increasing the number and size of cells and clear halo; increased endocytic organelles, and heterogeneous distribution of stereocilia, in animals with diet-induced obesity cafeteria. Given the results, it is believed that these changes should cause a profound impact on the luminal environment and interfere in the transport process, maturation, maintenance, protection and storage of sperm, being responsible for obesity alter the expression of AQP- 1 in efferent ducts, AQP- 9 in the epididymal cauda, the relative distribution of cells and clear halo and morphological characteristics of these parts via the sperm. However, more studies are needed to elucidate the specific mechanisms by which the cafeteria diet affects sperm morphology via specifically efferent ducts and epididymal ducts
A indução à obesidade, no modelo experimental animal com dieta de cafeteria, simula a alimentação com alto teor calórico que os seres humanos ingerem, na atualidade, possibilitando, assim, estudar a obesidade bem como as comorbidades advindas desta condição. O sistema genital masculino é afetado diretamente pela obesidade com aumento de peroxidação lipídica, aumento de corpos apoptóticos, mudanças nos parâmetros espermatobioscópicos e redução de fertilidade. O objetivo do estudo foi avaliar se há alterações causadas pela obesidade nos epitélios dos ductos eferentes e epididimário, tanto em relação à morfologia quanto à expressão de aquaporinas 1 e 9 (AQPs 1 e 9) em ratos Wistar adultos. Após o desmame, os animais foram divididos aleatoriamente em dois grupos: grupo controle (CON), que recebeu dieta padrão e água ad libitum (n=10) e grupo cafeteria (CAF), que recebeu dieta de cafeteria e refrigerante desgaseificado ad libitum (n=10). O tratamento do grupo CAF teve início depois da 12º semana de vida, totalizando 40 semanas de consumo da dieta de cafeteria, sendo todos os animais mortos com 52º semanas de idade. Os ductos eferentes, juntamente com segmentos inicial (Si), cabeça (Cç), corpo (Co) e cauda (Cd) do epidídimo, foram submetidos à rotina histológica e imunohistoquímica para AQP-1 e AQP-9. No presente estudo foram avaliados os dados: massa corporal, comprimento nasoanal, circunferência abdominal, índice de Lee e massa das gorduras retroperitoniais e perigonadais; também, avaliou-se dimensões, através de morfometria, e características morfológicas dos epitélios dos ductos eferentes e segmentos Si, Cç, Co e Cd do epidídimo, bem como foram analisadas as expressões de AQP-9 e AQP-1 nos ductos eferentes e segmentos epididimários supracitados. Alterações na expressão das AQPs, nos ductos eferentes e parte do epitélio epididimário, foram observadas com aumento na expressão de AQP-1 e redução de AQP-9 nos ductos eferentes e cauda epididimária, respectivamente, dos animais tratados com dieta de cafeteria. Também, ocorreram alterações morfológicas no epitélio epididimário, como aumento do número e tamanho de células halo e claras; aumento de organelas endocíticas; e distribuição heterogênea de estereocílios, nos animais com obesidade induzida por dieta de cafeteria. Em vista dos resultados, acredita-se que essas alterações devem causar um profundo impacto sobre o ambiente luminal e interferir no processo de transporte, maturação, manutenção, proteção e armazenamento dos espermatozoides, sendo a obesidade responsável por alterar a expressão de AQP-1 nos ductos eferentes, da AQP-9 na cauda epididimária, a distribuição relativa de células claras e halo e características morfológicas destas partes da via espermática. No entanto, mais estudos são necessários para esclarecer os mecanismos específicos pelos quais a dieta de cafeteria afeta a morfologia da via espermática, especificamente dos ductos eferentes e ductos epididimários
34
Debrand, Nicolas. "Caractérisation et étude d'un élément régulateur du gène codant pour le récepteur à la vasopressine de type 2." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2008. http://tel.archives-ouvertes.fr/tel-00485725.
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Le contrôle de la transcription constitue le principal niveau de la régulation de l'expression des gènes dans les cellules eucaryotes. Le laboratoire a identifié 6 familles indépendantes avec un diabète insipide néphrogénique (DIN) lié à l'X portant de grandes délétions en amont du gène de l'AVPR2. Dans chacune de ces familles, les gènes AVPR2 et AQP2 sont intacts et les hommes sont atteints de DIN lié à l'X dans sa forme rénale « classique ». Le séquençage et l'analyse de 61 kilobases en amont et en aval de l'AVPR2 ont permis l'identification de 6 zones délétées chez 6 familles indépendantes, dont 5 zones de taille supérieure à 7 kilo bases, et une zone, de 102 paires de bases, commune à l'ensemble des délétions. Chez le patient porteur de cette délétion, les récepteurs V2 ne sont pas exprimés dans le tubule collecteur mais le sont au niveau des cellules endothéliales. Notre travail est de tenter de comprendre les mécanismes régulateurs du locus de l'AVPR2, et d'étudier l'expression « tissu spécifique » de ce gène. Les études réalisées dans le système Hprt, confirment le rôle activateur de la séquence de 102 pb. Les expériences in vitro indiquent que cet effet dépende du contexte extracellulaire, de la nature des cellules, ainsi que du promoteur de l'AVPR2. Les protéines liant potentiellement l'une des extrémités de la délétion a révélé la présence, soit de protéines régulatrices, soit de séquences inconnues, toutes exprimées dans le rein. À terme, ces études, ainsi que celles en découlant, permettront de positionner l'AVPR2 comme une cible de choix dans le traitement des diabètes insipides, centraux et néphrogéniques, par thérapie génique.
35
Patyal, Pankaj. "Expression of Aquaporins in Mouse Choroid Plexus and Ependymal Cells." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1440892851.
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Grozman, Vladimir. "Evaluating the CU-tree algorithm in an HEVC encoder." Thesis, KTH, Skolan för datavetenskap och kommunikation (CSC), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-176054.
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CU-tree (Coding Unit tree) is an algorithm for adaptive QP (quantization parameter). It runs in the lookahead and decreases the QP of blocks that are heavily referenced by future blocks, taking into account the quality of the prediction and the complexity of the future blocks, approximated by the inter and intra residual. In this study, CU-tree is implemented in c65, an experimental HEVC encoder used internally by Ericsson. The effects of CU-tree are evaluated on the video clips in the HEVC Common test conditions and the performance is compared across c65, x265 and x264. The results are similar across all encoders, with average PSNR (peak signal-to-noise ratio) improvements of 3-10% depending on the fixed QP offsets that are replaced. The runtime is not impaired and improvements to visual quality are expected to be even greater. The algorithm works better at slow speed modes, low bitrates and with source material that is well suited for inter prediction.CU-tree är en algoritm för adaptiv QP. Den körs under framåtblicken (lookahead) och minskar QP för block som refereras av många framtida block, med hänsyn tagen till prediktionens kvalitet och de framtida blockens komplexitet, approximerat av inter- och intra-skillnaden. I denna studie implementeras CU-tree i c65, en experimentell videokodare som används internt på Ericsson. Effekterna av algoritmen utvärderas på videoklippen i HEVC Common test conditions och prestandan jämförs mellan c65, x265 och x264. Resultaten är liknande i alla videokodare, med genomsnittliga PSNR-förbättringar på 3-10% beroende på vilka fasta QP-offsets som algoritmen ersätter. Körtiden påverkas inte nämnvärt och den subjektiva kvaliteten förbättras troligen ännu mer. Algoritmen fungerar bättre med långsamma hastighetsinställningar, låg bitrate samt videoinnehåll som lämpar sig väl för inter-prediktion.
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Sene, Abdoulaye. "Caractérisation des complexes macromoléculaires Dp71-utrophine/DAPs responsables de l'agrégation des canaux Kir4. 1 at AQP4 dans la cellule gliale de Müller de la rétine : implications fonctionnelles." Paris 6, 2009. http://www.theses.fr/2009PA066225.
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La Dp71, un produit court du gène DMD (Dystrophie Musculaire de Duchenne) est une protéine intracellulaire du cytosquelette associé à la membrane et présentant le même patron d’expression que les canaux potassiques Kir4. 1 et aqueux AQP4 dans la cellule gliale de Müller (CGM) de la rétine. Nous avons identifié le complexe macromoléculaire qui se forme autour de la Dp71 et qui est responsable de la localisation et de l’agrégation des canaux Kir4. 1 et AQP4 dans la CGM. En utilisant la souris Dp71-null, nous avons pu étudier la composition du complexe se formant autour de l’utrophine en absence de la Dp71. Nous avons également étudié l’implication fonctionnelle des complexes autour de la Dp71 et de l’utrophine dans la régulation de l’homéostasie rétinienne à travers les CGM, dans un contexte normal et pathologique. Toutes ces données permettent de mieux comprendre le rôle de la Dp71 dans la distribution des canaux Kir4. 1 et AQP4 en des endroits précis de la membrane des CGM. De plus ces résultats soulignent l’importance de la Dp71 dans la modulation des caractéristiques morphologiques et fonctionnelles de la CGM en condition normale et pathologique.
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León, Rojas Gladys Daniela. "Mapeo de procesos de la Universidad AQP sede Arequipa y propuesta de tablero de mando integral para el proceso de enseñanza-aprendizaje." Master's thesis, Universidad Peruana de Ciencias Aplicadas (UPC), 2019. http://hdl.handle.net/10757/626594.
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Se propone en este trabajo el Tablero de Mando Integral (con sus indicadores) y la mejora de procesos del Macroproceso de Enseñanza-Aprendizaje de una filial universitaria ubicada en la ciudad de Arequipa (por temas de confidencialidad hemos tenido que cambiar el nombre de ésta a Universidad AQP).
El rápido y desordenado crecimiento de esta filial hacia urgente contar con una herramienta integrada de control al menos para el principal proceso de negocio (Enseñanza-Aprendizaje). Igualmente era importante eliminar reprocesos e ineficiencias dentro de este macroproceso.
Producto del análisis interno y externo realizado se ha elaborado la propuesta de Tablero de Mando Integral y sus indicadores como una herramienta de control y gestión de la estrategia de esta filial tomada en este trabajo como una unidad de negocio.
Para la mejora de sus procesos se ha sugerido reforzar la autonomía de la sede Arequipa de la Universidad AQP para aportar flexibilidad y eficiencia a sus operaciones. Otra importante mejora sugerida es la implementación de una plataforma tecnológica (software) para el soporte administrativo vinculado al macroproceso de Enseñanza-Aprendizaje (Planificación automatizada de cursos, horarios, aulas, docentes y evaluaciones, entre otros).The Balanced Scorecard (with its indicators) and the process optimization of the Teaching-Learning Macroprocess of a university subsidiary located in the city of Arequipa are proposed in this work (for confidentiality reasons we have had to change the name of this AQP University). The rapid and messy growth of this subsidiary made it urgent need for an integrated control tool at least for the main business process (Teaching-Learning). It was also important to eliminate reprocesses and inefficiencies within this macroprocess. As a result of the internal and external analysis carried out, the proposal of the Balanced Scorecard and its indicators has been prepared as a tool for controlling and managing the strategy of this subsidiary taken in this work as a business unit. For the improvement of its processes it has been suggested to strengthen the autonomy of the Arequipa headquarters of the AQP University to provide flexibility and efficiency to its operations. Another important improvement suggested is the implementation of a technological platform (software) for administrative support linked to the Teaching-Learning macroprocess (automated planning of courses, schedules, classrooms, teachers and evaluations, among others).
Tesis
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Debrand, Nicolas. "Caractérisation et étude d’un élément régulateur du gène codant pour le récepteur à la vasopressine de type 2." Paris 6, 2008. https://tel.archives-ouvertes.fr/tel-00485725.
Full textAbstract:
Le laboratoire a identifié 6 délétions en amont du gène de l’AVPR2, dont une de 102 paires de bases commune à chaque délétion, chez 6 familles indépendantes atteintes de diabète insipide néphrogénique (DIN) lié à l’X. Dans chacune de ces familles, les gènes AVPR2 et AQP2 sont intacts et les hommes sont atteints de DIN lié à l’X dans sa forme rénale « classique ». Chez le patient porteur de cette délétion, les récepteurs V2 ne sont pas exprimés dans le tubule collecteur mais le sont au niveau des cellules endothéliales. Nous avons étudié la régulation du locus de l’AVPR2, et l’expression « tissu spécifique » de ce gène. Les études confirment le rôle activateur de la zone de 102 pb en indiquant que cet effet dépend du contexte extracellulaire, de la nature des cellules, ainsi que du promoteur du gène. Ces études permettront de positionner l’AVPR2 comme une cible de choix dans le traitement des diabètes insipides par thérapie génique
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Ceperuelo, Mallafré Mª Victòria. "Estudi del canal de glicerol aqp7 i de l'adipoquina zag en l'àmbit de l'obesitat, la diabetis tipus 2 i la síndrome metabòlica. Dues proteïnes implicades en la lipòlisi del teixit adipós." Doctoral thesis, Universitat Rovira i Virgili, 2010. http://hdl.handle.net/10803/8883.
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L'obesitat incrementa les possibilitats de patir altres malalties com la diabetis mellitus tipus 2 (DM2), la dislipèmia, la hipertensió, entre d'altres. Per tal de poder avançar en noves dianes terapèutiques que millorin aquestes malalties és necessari conèixer millor la biologia del teixit adipós i els seus components. El teixit adipós blanc, a més a més d'emmagatzemar la major part de les reserves energètiques, és capaç de tenir activitat metabòlica i endocrina. Cal tenir en compte que un adequat metabolisme lipídic en l'adipòcit és clau també per aconseguir un equilibri en l'homeòstasi del metabolisme glucídic en l'ésser humà. En aquest treball hem analitzat el paper de dues proteïnes implicades en la lipòlisi del teixit adipós, d'una banda el canal de glicerol aquaporina 7 (AQP7) i per altra l'adipoquina glicoproteïna Zinc-α 2 (ZAG), en el context de l'obesitat, la síndrome metabòlica i la DM2.Així, en aquesta tesi doctoral, hem pogut arribar a les següents conclusions:
1. L'expressió del canal de glicerol AQP7, en teixit adipós, es troba disminuïda en pacients afectes d'obesitat mòrbida.
2. La DM2 no sembla afectar l'expressió d'aquesta aquagliceroporina en el teixit adipós.
3. Ambdues aquagliceroporines, AQP7 (al teixit adipós) i AQP9 (al teixit hepàtic) mantenen un estreta relació en pacients obesos mòrbids.
4. La glicoproteïna Zinc-α 2 (ZAG) sembla tenir un paper rellevant en l'homeòstasi del teixit adipós amb un fort lligam amb altres adipoquines, especialment l'adiponectina.
Obesity increases the chances to suffer from other diseases such as type 2 diabetes mellitus (T2DM), hyperlipidemia, hypertension, and others. In order to get into new therapeutic targets to improve these conditions, a best knowledge of the biology of adipose tissue and its components is needed. In addition to storing the most of energy reserves, white adipose tissue is able to have metabolic and endocrine activity. It is necessary to consider that an appropriate lipid metabolism in the adipocyte is also essential to achieve a balance in the homeostasis of glucose metabolism in humans. In this study we have examined the role of two proteins involved in adipose tissue lipolysis, first glycerol channel aquaporin 7 (AQP7) and on the other hand adipokine Zinc-α 2 glycoprotein (ZAG), in the context of obesity, metabolic syndrome and T2DM. Thus, in this thesis, we have reached the following conclusions:
1. The glycerol's channel AQP7 expression, in adipose tissue, is decreased in patients with morbid obesity.
2. The DM2 does not appear to affect the expression of this aquaglyceroporin in adipose tissue.
3. Both aquaglyceroporins, AQP7 (in adipose tissue) and AQP9 (in liver tissue) have a close relationship in morbidly obese patients.
4. The Zinc-α 2 glycoprotein (ZAG) seems to play an important role in the homeostasis of adipose tissue with a strong bond with other adipokines, particularly adiponectin.
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Munger, Emily LaRee. "Alteration to Astrocyte Density and Morphology across Mammalia with Specific Attention to Primate Brain Evolution and Aging." Kent State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=kent1594638449298271.
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Rurak, Jennifer Mary Elizabeth. "Implications of alpha-dystroglycan glycosylation in the proper assembly of the dystroglycan associated protein complex and the polarized distribution of the inwardly rectifying potassium channel, Kir4.1, and the water permeable channel, AQP4, in perivascular glia." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/32339.
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The dystroglycan protein complex spans the plasma membrane and provides a link
between the cytoskeleton and the extracellular matrix (ECM). Defective O-linked
glycosylation of α-dystroglycan (α-DG) within the complex severs this link leading to a
subset of muscular dystrophies known as the dystroglycanopathies. These are
characterized by muscle weakness and degeneration as well as by brain and ocular
defects of unknown etiology. In brain and retina, α-DG and ECM molecules are enriched
at astrocytic domains abutting blood vessels where they may be involved in localizing the
inwardly rectifying potassium channel, Kir4.1, and aquaporin channel, AQP4, to
astrocytic endfeet. To investigate the role of ECM ligand-binding to glycosylated sites on
α-DG in the polarized distribution of these channels in vivo, we used the Large [superscript] myd mouse,
an accepted animal model for dystroglycanopathies. We found that Kir4.1 and AQP4 are
lost from astrocytic endfeet in brain while significant labeling for these channels is still
detected at analogous cell domains in retina. Furthermore, while both α- and β₁-
syntrophins are lost from perivascular astrocytes in brain of the Large [superscript] myd mouse, labeling
for β₁-syntrophin is still evident at parallel domains in retina. These findings show that
while ligand-binding to glycosylated sites on α-DG in concert with α- and β₁-syntrophins
is crucial for the polarized distribution of Kir4.1 and AQP4 to functional domains in
brain, distinct mechanisms may contribute to their localization in retina.Medicine, Faculty of
Graduate
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Elster, Judith. "Die Bedeutung von Aquaporin1- und Aquaporin4-Konzentrationen im Liquor cerebrospinalis für Patienten mit Normaldruckhydrozephalus und Pseudotumor cerebri." Doctoral thesis, 2011. http://hdl.handle.net/11858/00-1735-0000-0006-B2A5-4.
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Nešverová, Veronika. "Studie interakce mezi lidským AQP5 a PIP." Master's thesis, 2014. http://www.nusl.cz/ntk/nusl-337395.
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Charles University in Prague Faculty of Pharmacy in Hradec Králové Department of Biochemical Sciences University of Gothenburg Faculty of Science Department of Chemistry and Molecular Biology Candidate: Veronika Nešverová Supervisor: Vladimír Wsól Title of diploma thesis: Studies of the interaction between human AQP5 and PIP Aquaporin 5 is a membrane canal which maintains water balance mainly in lacrimal and salivary glands. A defect in this protein's trafficking from cytoplasm to cytoplasmic membrane is thought to play a role in development of Sjögren's syndrome - a chronic autoimmune disease. Prolactin-inducible protein is a cytoplasmic protein which was found to be contributing to this disease's pathogenesis. This project was aimed to study the proposed interaction between aquaporin 5 and prolactin-inducible protein. Both recombinant proteins were overexpressed in the yeast Pichia pastoris and purified using low-pressure column chromatography on an ÄKTA purification system. Glycosylation of prolactin-inducible protein was confirmed using specific glycoprotein staining. Two coelution tries were run on a HisTrap column. The fractions eluted from the second try were analysed by mass spectrometry. However results did not confirm any interaction. Further investigation is needed for the complete...
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Faria, Nuno Filipe Machado. "AQP4-seronegative patients with a neuromyelitis optica phenotype." Master's thesis, 2016. https://repositorio-aberto.up.pt/handle/10216/90207.
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Faria, Nuno Filipe Machado. "AQP4-seronegative patients with a neuromyelitis optica phenotype." Dissertação, 2016. https://repositorio-aberto.up.pt/handle/10216/90207.
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"A WATER CHANNEL (AQP9) IN RETINAL GANGLION CELL APOPTOSIS AND GLAUCOMA." Texas Christian University, 2007. http://etd.tcu.edu/etdfiles/available/etd-04202007-153701/.
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Iandiev, Ianors. "Differential regulation of Kir4.1 and AQP4 in the postischemic rat retina /." 2004. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=013193554&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
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Cheng, Chu-Jung, and 鄭竹容. "Effects of increased hydrostatic pressure on cell migration:Roles of Aquaporin1 (AQP1) activation." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/u546hw.
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碩士國立臺灣大學
生醫電子與資訊學研究所
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Mechanical cues from microenvironment of cells have a great influence on the cell’s behaviors. Many solid tumors are characterized by high interstitial fluid pressure (IFP), which leads to a reduced uptake of therapeutic drugs or antibodies into the tumors and results in a significant obstacle in cancer therapy. However, whether the increased IFP plays a direct role in behaviors of cancer cells remains unclear. Understanding of relationships between the increased IFP and cancer cell’s behaviors holds the promise of improvement of strategies for cancer therapy. In this work, we developed a cell-culturing system that imposed various hydrostatic pressures (HPs) ranging from 0 to 20 mmHg on cultured cells to simulate the increased IFP and examined the changes in cell’s behaviors. We found that high HP enhances the migration speed, spreading area, number of filopodia, and volume of individual lung cancer cells. By contrast, those changes in normal lung cells were not significant after exposure to high HP. Biochemical studies using western blotting revealed that high HP promoted motility of lung cancer cells via ERK1/2-mediated activation of aquaporin-1 (AQP1), whereas high HP elicited minimal changes in cell motility and morphology in normal lung cells. Our data indicate that high HPs significantly change the invasiveness of lung cancer cells and highlighted the role of ERK1/2-dependent activation of AQP1 in these changes.
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De, Ieso Michael Lucio. "Pharmacological Modulation of Cancer Migration and Invasion Through Targeting AQP1 Ion and Water Channel Activity." Thesis, 2019. http://hdl.handle.net/2440/120206.
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Cancer invasion and metastasis are the leading causes of cancer-related deaths. Aquaporin-1 is a dual water and ion channel that is upregulated in many aggressive cancers including colon, breast, and brain cancer; aquaporin-1 enhances cell migration, invasion and metastasis in these cancer types. Other aquaporins with water channel function are not able to substitute for aquaporin-1 in facilitating cell migration. There is a gap in knowledge regarding the properties of aquaporin-1 that permit its migration-enhancing effect, but both the ion and water channel activities appear to be involved. Thus, it was hypothesised that aquaporin-1 water and ion channels exhibit a coordinated role in aquaporin-1-facilitated cancer cell motility. The aims of this thesis were to test whether pharmacological block of the aquaporin-1 water and ion channel would impede cell migration and invasion in aquaporin-1-expressing cancer cell lines, and to see if the efficacy of aquaporin-1 inhibitors depended on membrane localisation of the channel. Proposed aquaporin-1 blocker AqB050, AQP1 water channel blocker bacopaside II, and an aquaporin-1 ion channel blocker AqB011 were used. The circular wound closure assay is an innovative alternative approach for measuring cell migration and was introduced and utilised in this thesis. Cell viability and proliferation was quantified using an alamarBlue assay. Cell invasion was measured with the transwell assay. Glioblastoma, colorectal adenocarcinoma, and mammary gland tumour cell lines were used. Results showed that combined pharmacological inhibition of aquaporin-1 water and ion conductance amplified the block of cancer cell migration as compared to block by each inhibitor alone, suggesting a cooperative role of aquaporin-1 water and ion channels in cell migration. Cancer cells that express aquaporin-1 on the membrane were more sensitive to block by aquaporin-1 inhibitors; this could be an important screening tool for identifying cancer subtypes likely to respond to AQP1 inhibitors. AqB011 and AqB050 inhibited glioblastoma, breast and colon cancer invasiveness. A newly generated mixture of compounds (AqB051) containing the proposed AQP1 blocker AqB050 and related derivatives was found to strongly block cancer transwell invasion. The potent biologically active agent (not AqB050) was then narrowed to one fraction (fraction E) from AqB051. AqB051 and fraction E significantly inhibited invasiveness in all glioblastoma cell lines. Work in this thesis paves the way for improving methods utilized for measuring cell migration, investigating the role of AQP1 ion conductance and subcellular localisation in cancer migration and growth, investigating a novel and potent inhibitor for glioblastoma invasion, and testing the effects of AQP1 modulators in treating other non-neoplastic diseases.Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2019