Dissertations / Theses: 'Hormone proteine'

1

Aina, E. M. "Regulation du metabolisme du glucose et des acides amines par l'insuline et le glucagon chez la chevre en lactation." Clermont-Ferrand 2, 1988. http://www.theses.fr/1988CLF21126.

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2

Beau, Isabelle. "Etude de la polarisation des récepteurs de la FSH de la LH et de la TSH dans les cellules MDCK." Paris 11, 1995. http://www.theses.fr/1995PA11T035.

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3

Pascalon, Annette. "Influence des deficits energetiques et proteiques sur l'evolution de la gestation et le taux des acides amines libres chez la ratte : effets sur les concentrations de progesterone et de prolactine aux periodes critiques de la mortalite embryonnaire." Clermont-Ferrand 2, 1988. http://www.theses.fr/1988CLF21092.

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4

Samson, Michel. "Le transport membranaire des hormones thyroïdiennes : caractérisation, identification et purification partielle des protéines de transport de l'érythracyte." Paris 11, 1993. http://www.theses.fr/1993PA11T035.

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5

Crave, Jean-Charles. "Proteine de liaison des hormones steroides sexuelles ; role des facteurs metaboliques et nutritonnels." Lyon 1, 1990. http://www.theses.fr/1990LYO1M182.

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6

Cousin, Patrice. "Étude des formes circulantes de la Sex Hormone-Binding Globulin (SHBG) humaine, protéine de liaison des hormones stéroïdes sexuelles : mesure des clairances métaboliques." Lyon 1, 2000. http://www.theses.fr/2000LYO1T006.

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7

Desvergne, Béatrice. "Regulation transcriptionnelle par les hormones thyroidiennes : caracterisation des elements de reponse presents au sein des promoteurs des genes de l'enzyme malique et de la proteine basique de la myeline." Paris 11, 1993. http://www.theses.fr/1993PA11T033.

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8

David, Jean-Pierre. "Régulation hormonale du promoteur de la HSP90 de poulet : modulation de la réponse hormonale par le choc thermique." Paris 11, 1992. http://www.theses.fr/1992PA11T016.

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9

Dinerstein-Cali, Hélène. "Etude des molecules impliquees dans la transduction du signal du recepteur de l'hormone de croissance (doctorat : endocrinologie et interactions cellulaires)." Paris 11, 2000. http://www.theses.fr/2000PA11T005.

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10

Le, Bihan Stéphane. "Role des immunophilines dans le mecanisme d'action des recepteurs des glucocorticosteroides et des progestagenes." Paris 11, 1996. http://www.theses.fr/1996PA11T025.

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11

Santa, Barbara Pascal de. "Régulations transcriptionnelles de l'hormone anti-müllerienne et de son récepteur au cours du développement embryonnaire humain." Montpellier 1, 1998. http://www.theses.fr/1998MON1T018.

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12

VIE, MARIE-PIERRE. "Une proteine de liaison de haute affinite des hormones thyroidiennes : caracterisation, identification, purification et clonage moleculaire (doctorat : biochimie et biologie moleculaire)." Paris 11, 1998. http://www.theses.fr/1998PA11T014.

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13

Tronik, Le Roux Diana. "Regulation genetique et hormonale de la synthese de renine et de la proteine smr1 chez la souris et le rat." Paris 7, 1988. http://www.theses.fr/1988PA077163.

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Biosynthese et expression genique de renin dans la glande sousmaxillaire. Caracterisation d'une proteine smr1 tres abondante chez le rat male et absente chez la femelle. Les proteines de la glande sousmaxillaire du rat ne sont pas homologues de celles de la souris

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14

Ferment, Olivier. "Retrocontrole du magnesium sur la secretion de l'hormone parathyroidienne et de la calcitonine chez l'homme sain : etude comparee avec le calcium et aspects chronopharmacologiques." Paris 6, 1987. http://www.theses.fr/1987PA066090.

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15

Puccio, François. "Influence de l'hydrocortisone, de l'egf, de la bombesine et du grf sur la proliferation cellulaire et la maturation du tractus gastrointestinal et du pancreas chez le jeune rat non sevre." Paris 6, 1988. http://www.theses.fr/1988PA066497.

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16

Fraboulet, Sandrine. "Mecanismes de regulation de la peptidylglycine alpha-amidating monooxygenase (pam) par les hormones thyroidiennes (doctorat)." Aix-Marseille 2, 1997. http://www.theses.fr/1997AIX20652.

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17

Leturque, Armelle. "Adaptations du métabolisme glucidique pendant la gestation chez la ratte." Paris 7, 1985. http://www.theses.fr/1985PA077060.

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Durant la gestation, des modifications physiologiques et métaboliques importantes interviennent dans le compartiment maternel liées à l'apparition de novo des foetus et des placentas. Le foetus consomme, en tant que substrat énergétique essentiel, une quantité croissante du glucose. Quant au placenta, il contrôle le transfert de glucose au foetus et secrète des hormones favorisant la production d'insuline par le pancréas maternel. Les adaptations du métabolisme glucidique maternel seront donc nombreuses. Le but de notre travail a été de définir au cours de la gestation chez la ratte les mécanismes par lesquels l'homéostasie glucidique est maintenue face à une dépense énergétique intense et de quantifier les besoins en glucose de chaque tissu. Nous avons aussi défini et quantifié la résistance à l'insuline qui s'établit pendant la gestation et nous nous sommes demandés quels étaient les tissus et les mécanismes impliqués. Chez la ratte une étude de l'évolution de la glycémie au cours de la gestation mise en parallèle avec l'évolution du poids du conceptus montre 1) qu'à 14 jours de gestation une hypogly¬cémie post-absorptive est observée alors que le conceptus repré¬sente seulement 4 % du poids de la mère, 2) que durant la dernière semaine de gestation la glycémie diminue légèrement alors que le conceptus est en phase exponentielle de croissance. Nous en avons conclu que l'hypoglycémie de la gestation n'était pas due à une consommation importante de glucose par le conceptus.

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18

Barrault, Valérie. "Les protéines kinases C : mise au point du dosage et valeurs basales dans divers modèles expérimentaux." Paris 5, 1992. http://www.theses.fr/1992PA05P083.

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19

Elboury-Elouardirhi, Houria. "Étude sur les régulations, par des protéines non histones de l'expression du gène de l'hPL dans le placenta humain." Nancy 1, 1988. http://www.theses.fr/1988NAN10264.

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La concentration élevée de l'hPL dans la plasma de la femme enceinte, en fin de grossesse, sa sécrétion placentaire estimée à plus de 1 gramme par 24 heures, son pourcentage appréciabvle de l'ensemble des protgéines placentaires, sa structure composée d'une simple chaîne d'acides aminés, sans participation de résidus glycosylés ou phosphorylés, les inconnues actuelles concernant les mécanismes de régulation de sa production, sont les facteurs qui nous ont déterminé à réaliser sa synthèse in vitro

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20

Murakaeva, Asiya. "Structure, evolution and expression of the duplicated growth hormone genes of common carp (Cyprinus carpio)." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15982.

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Der Karpfen, Cyprinus carpio, ist eine tetraploide Fischart aus der Familie Cyprinidae, die vor 20-50 Mio Jahren entstanden ist. Das Ziel der vorliegenden Arbeit war der Versuch, die funktionelle Rolle der duplizierten GH Gene des Karpfens durch das Studium ihrer Struktur, Evolution und Expression zu verstehen. Die Introns des zweiten GH Gens des Karpfens wurden erstmalig sequenziert und Sequenzvergleiche der kodierenden und nicht-kodierenden Bereiche von Allelen beider GH Gene wurden vorgenommen. Eine phylogenetische Analyse wurde durchgefuhrt, um die Beziehungen der GH Gene des Karpfens zu denen des tetraploiden Goldfischs und anderer diploider Cypriniden zu untersuchen. Zusatzlich wurden weitere duplizierte Gene des Karpfens, von denen einige auch fur das Wachstum von Bedeutung sind, phylogenetisch analysiert. Der Test der relativen Evolutionsrate nach Tajima (1993) zeigte einen statistisch signifikanten Anstieg der Evolutionsrate des GH I Gens beim Karpfen. Es wurden in der vorliegenden Arbeit einige weitere duplizierte Genpaare des Karpfens und Goldfischs gefunden, die ebenfalls eine Lockerung funktioneller Zwange oder sogar Beweise fur positive Darwin?sche Selektion bei einem der beiden Duplikate zeigen. Der Expressionstest hat gezeigt, dass die GH I und GH II Gene auf identischen Niveaus bei Karpfenbrut exprimiert werden, wahrend bei ein Jahr alten Karpfen, drei Jahre alten Mannchen und Weibchen sowie den 10 Monate alten, an kalte Temperaturen (2°C) angepassten Fischen die Expression von GH II statistisch signifikant geringer war als die von GH I. Es wurde eine neue und einfache Methode zur Herstellung von rekombinanten, biologisch aktiven GH-Proteinen ohne Notwendigkeit des Refolding entwickelt. Sie ermoglicht spatere Tests, ob die Aktivitat von unterschiedlichen GH-Varianten des Karpfens gleich oder unterschiedlich ist.
The common carp, Cyprinus carpio, is a tetraploid fish species from the family Cyprinidae that arose about 20-50 Myr ago. The aim of the present work was attempting to understand the functional role of the duplicated common carp GH genes by studying their structure, evolution and expression. The introns of the second GH gene of common carp were sequenced for the first time and sequence comparisons of coding and non-coding regions of alleles of both GH genes were carried out. A phylogenetic analysis was done to examine the relationships of common carp GH genes with GH genes of the tetraploid goldfish and other diploid Cyprinids. In addition, phylogenetic analyses were done with other duplicated genes of common carp, some of which also important for growth. The relative rate test of Tajima (1993) showed a statistically significant increase in the evolution rate of the common carp GH I gene. In addition, some other duplicated gene pairs in common carp and goldfish with relaxation of functional constraints or even evidence of positive Darwinian selection in one of the two gene duplicates were found in the present study. The test of expression rates of the two GH genes has shown that the GH I and GH II genes were expressed at similar levels in carp fry. In contrast, the expression of GH II was statistically significantly lower than that of GH I in one year old carp, three years old males and females as well as in 10 months old fish adapted to cold temperature (2°C). To enable testing the hypothesis if activity of GH diverged between different GH variants of common carp a new and simple method for production of recombinant, biologically active GH proteins without the necessity of refolding was developed.

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21

Landron, Dorothée. "Interactions de l'hormone de croissance humaine avec les adipocytes de rats zucker genetiquement obeses : relations entre la liaison et les effets biologiques." Paris 6, 1988. http://www.theses.fr/1988PA066344.

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L'objectif de ce travail est de comparer la liaison et les effets biologiques de l'hormone de croissance (gh) 1) dans les adipocytes du tissu inguinal de jeunes rats zucker obeses fa/fa et minces fa/fa; 2) dans les preadipocytes de rats zucker en culture primaire au cours de la differenciation adipocytaire. 1. Les etudes de liaison de la gh et les courbes dose-reponse pour le transport et le metabolisme du glucose sont realisees avec des adipocytes soit fraichement isoles (f) soit preincubes 3 h (p)

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22

RIAD, FOUAD. "Regulation endocrinienne de la secretion salivaire des mineraux chez les bovins." Clermont-Ferrand 2, 1986. http://www.theses.fr/1986CLF21026.

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23

Soubigou, Pascal. "Cycle du recepteur de l'insuline et devenir de l'hormone chez l'hepatocyte foetal en culture : relation avec la reponse glycogenique a l'insuline." Paris 6, 1987. http://www.theses.fr/1987PA066214.

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24

Stevens, Jeffrey David. "LHRH fusion protein vaccines in beef heifers and bovine ectopic ovarian xenografting." Online access for everyone, 2004. http://www.dissertations.wsu.edu/Dissertations/Fall2004/J%5FStevens%5F092204.pdf.

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25

Fafeur, Véronique. "Rôle des métabolites de l'acide arachidonique et en particulier de la prostaglandine E2 dans la sécrétion de l'hormone de croissance : implication dans le mécanisme d'action du facteur hypothalamique de libération de l'hormone de croissance." Paris 6, 1986. http://www.theses.fr/1986PA066205.

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L’hypothèse d'un effet stimulant de la PGE2 sur la libération hypothalamique de R-GRF n'est pas confirmée. Au niveau hypophysaire, la PGE2 et la GRF agissent par des voies convergentes pour stimuler la GH. La synthèse de PGE2 est induite par le GRF et les inhibiteurs du métabolisme de l'acide arachidonique diminuent la libération de GH induite par le GRF, suggérant un rôle modulateur de la PGE2 dans l'action du GRF. La présence des récepteurs spécifiques à la PGE2 au niveau des cellules hypopohysaires et l'activation de la PGE2 endogène par le GRF suggèrent une régulation autocrine et non ou paracrine amplifiant la sensibilité de cellules somatotrophes au GRF. Les produits de la voie lipoxygènase et non ou epoxygènase paraissent également impliquées. La mise en jeu de mécanismes intracellulaires dépendants du calcium, parallèlement à l'activation des cyclases par le GRF est confirmée.

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26

Sai, Pierre. "Etude de l'auto-immunite dirigee contre les cellules pancreatiques a insuline au cours des diabetes insulinoprives." Nantes, 1987. http://www.theses.fr/1987NANT2062.

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Pathogenie autoimmune des diabetes insulinoprives chez l'homme, la souris et le rat. Des lymphocytes circulants alterent in vitro l'insulinosecretion des cellules d'ilots et peuvent presenter des anomalies du circuit de l'interleukine 2. Essai d'immunotherapie par la ciclosporine a

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27

Duvic, Bernard. "Purification et etude de la proteine de transport de la 20-hydroxyecdysone chez un insecte : locusta migratoria." Université Louis Pasteur (Strasbourg) (1971-2008), 1988. http://www.theses.fr/1988STR13160.

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La purification du transporteur est realisee a partir d'hemolymphe par differentes techniques (coagulation a temperature ambiante; chromatographie sur colonne echangeuse d'anions; chromatographie sur colonne de gel permeation; hplc sur phase echangeuse d'anions). Le transporteur est une glycoproteine acide (pi=5,6) de 280 kda. C'est un homodimere a 2 sous-unites de 140 kda dont la sequence n-terminale a ete determinee. Un polyserum de lapin et 2 anticorps monoclonaux de souris ont ete obtenus et permettent un dosage elisa du transporteur. Des dosages chez l. M. Montrent que le transporteur et l'ecdysone varient dans le meme sens. L'injection massive d'ecdysone suggere une synthese du transporteur sous le controle des ecdysteroides

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28

BERNARD, DOMINIQUE. "Expression des antigenes hla-dr par le tissu mammaire dans les cancers du sein." Clermont-Ferrand 2, 1986. http://www.theses.fr/1986CLF2E367.

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Mise au point d'une technique permettant le masquage de l'anticorps monoclonal anti hla-dr et de l'antigene hla-dr des cellules, l'immunoprecipitation des antigenes hla-dr, l'isolement de l'immun complexe et sa quantification par chromatofocusing. Mise en evidence de la regulation hormonale de l'expression des antigenes: en particulier role de la prolactine de l'oestradiol et de la progesterone. Effets de la gestation et de la lactation. Travail effectue sur la tumeur mammaire chimio-induite par la n-nitroso-n-methyluree chez la rate ainsi que sur un modele tumoral humain: la lignee mcf7

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29

Pere, Marie-Christine. "Adaptations du metabolisme hepatique chez la lapine en fin de gestation." Paris 6, 1987. http://www.theses.fr/1987PA066575.

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30

Debuyser, Anne. "Etude du controle noradrenergique de la cellule beta du pancreas de souris par des techniques electrophysiologique, radioimmunologique et radioisotopiques." Poitiers, 1988. http://www.theses.fr/1988POIT2324.

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31

Morel, Frédéric. "Etude experimentale du controle d'une famille de proteines de secretion d'un organe androgeno-dependant : l'epididyme de lezard." Clermont-Ferrand 2, 1987. http://www.theses.fr/1987CLF21074.

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32

Perrin, Dominique. "Role de la fodrine dans les cellules chromaffines de la medullo-surrenale." Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR13087.

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La membrane des granules de secretion des cellules chromaffine est capable de gelifier l'actine de facon calcium dependante. Le facteur de gelation associe a la membrane est la godrine, proteine de la famille de la spectrine. L'auteur demontre que la godrine est impliquee dans le processus de liberation des catecholamines, les proteines contractiles etant impliquees dans ce phenomene

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33

Kergoat, Micheline. "Secretion et mode d'action de l'insuline dans un modele de diabete non-insulinodependant chez le rat." Paris 7, 1988. http://www.theses.fr/1988PA077085.

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34

Cowan, Jon Walter. "Proteolysis and the growth hormone receptor identification and characterization of GHR as a [gamma]-secretase substrate /." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/cowan.pdf.

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35

Cziko, Paul. "Molecular Physiological Evolution: Steroid Hormone Receptors and Antifreeze Proteins." Thesis, University of Oregon, 2015. http://hdl.handle.net/1794/18733.

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For my dissertation research I explored the diversity and functional evolution of steroid hormone receptors (SRs) in animals and the physiological implications of the evolution of antifreeze proteins in Antarctic notothenioid fishes. For the former, I discovered multiple new SRs from the vast and under-sampled swath of animal diversity known as invertebrates. I used the sequences of these and other newly discovered related receptors in combination with genomic data and molecular phylogenetic techniques to revise the understanding of the evolutionary history of this important gene family. While previous studies have suggested that vertebrate SR diversity arose from a gene duplication in an ancestor of all bilaterian animals, my work presents strong evidence that this duplication occurred much later, at the base of the chordates. Furthermore, to determine the implications of added diversity and a revised phylogeny on inferences of the functional evolution of SRs, I functionally characterized heretofore-unknown SRs from hemichordates, an acoelomate flatworm, and a chaetognath and statistically reconstructed and functionally characterized ancestral SRs. My results expand the known sequence and functional repertoire of SRs in animals while reinforcing the previous inference that all SRs evolved from an estrogen-sensitive ancestral receptor. I also explored the consequences of the evolution of antifreeze proteins in Antarctic notothenioid fishes, a crucial adaptation to their icy, polar environment. These special proteins adsorb to ice crystals that enter a fish's body and prevent further growth, thereby averting death. I discovered that, in addition to their lifesaving growth-inhibiting ability, AFPs also prevent the melting of internal ice crystals at temperatures above the expected equilibrium melting point. Together with a decade-long temperature record of one of the coldest fish habitats on earth, my experimental results show that the evolution and expression of antifreeze proteins is accompanied by a potentially detrimental consequence: the lifelong accumulation of ice inside these fishes' bodies. This dissertation includes previously published co-authored material as well as unpublished co-authored material.
2017-01-14

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36

Benedet, Perea Susana. "Growth hormone and somatolactin function during sexual maturation of female Atlantic salmon /." Göteborg : Göteborg University, Department of Zoology/Zoophysiology, 2008. http://gupea.ub.gu.se/dspace/bitstream/2077/18305/4/gupea_2077_18305_4.pdf.

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37

Roblin, Sylvie. "Isolement et caractérisation d'une protéine de liaison cytosoluble intervenant dans la régulation des stéroïdes sulfatases membranaires." Besançon, 1988. http://www.theses.fr/1988BESA2029.

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38

Jacquot, Jacky. "Proteines des secretions bronchiques humaines : isolement, caracterisation et fonctions du lysozyme." Reims, 1987. http://www.theses.fr/1987REIMS002.

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Le lysozyme est localise au niveau des granules secretoires dans les cellules sereuses des glandes sous-muqueuses de la trachee humaine. Le lysozyme bronchique humain presente des effets bacteriostatiques et bacteriolytiques plus important vis-a-vis du pneumocoque streptococcus pneumoniae, germe frequemment responsable de certaines pathologies infectieuses respiratoires

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39

Babin, Patrick. "Lipoproteines et apolipoproteines plasmatiques chez les poissons teleosteens." Paris 6, 1987. http://www.theses.fr/1987PA066032.

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Caracterisation des lipoproteines plasmatiques et de leurs apolipoproteines chez salmo gairdneri. Determination de leur masse moleculaire et de leur densite. L'etude au long du cycle annuel de reproduction a permis de demontrer la presence de proteines vitellines ovulaires dans le plasma. De plus, le role des lipoproteines, plasmatiques dans la steroidogenese ovarienne a ete etudie

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40

Abbott, Mary-Alice. "Structural and Signaling Proteins at the Synapse: Dystroglycan & Insulin Receptor Tyrosine Kinase Substrate p58/53: a Dissertation." eScholarship@UMMS, 1999. https://escholarship.umassmed.edu/gsbs_diss/124.

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The synapse is the primary locus of cell-cell communication in the nervous system. The elaboration of a functional synapse requires both a specialized structure and an efficient communication system. For my thesis work, I studied proteins implicated in each of these functions: the structural molecules dystroglycan and dystrophin, and the signaling elements Insulin Receptor Substrate p58/53 and insulin receptor. The α/β-dystroglycan complex, believed to be the heart of cellmatrix adhesion in muscle and other tissues, provides a link between dystrophin, a cytoskeletal protein at the base of the muscle cell's Dystrophin Associated Protein Complex, and the extracellular matrix. In addition, dystrophin is found at central synapses, tightly associated with the postsynaptic density. The absence of dystrophin and the secondary loss of its associated proteins causes the genetic disease Duchenne Muscular Dystrophy. DMD affects both muscle and brain, causing a severe muscular dystrophy and lower IQs than control groups. In the first portion of my thesis work, I sought to determine the role of dystroglycan, dystrophin's peripheral partner, at central synapses. I probed Northern blots of brain regions to delineate the distribution of brain β-dystroglycan mRNA and to uncover any β-dystroglycan-related transcripts in brain. Then, using subcellular brain fractions, and cultured hippocampal neurons, I determined that whereas α-dystroglycan is associated with central synapses, β-dystroglycan is not. This discovery is surprising, and differs from the finding that dystrophin and α- and β-dystroglycan colocalize at the presynaptic membrane of retinal photoreceptors. In the course of the above mentioned work, using the anti-β-dystroglycan antiserum Ab98, I discovered a pair of proteins that were tightly associated with the postsynaptic density. These polypeptides of 58 kDa and 53 kDa (p58/53) were highly enriched in postsynaptic density (PSD) fractions from rat cerebral cortex, hippocampus, and cerebellum. In pursuit of a potential synapse-specific dystroglycan relative, I purified p58 and p53 by a combination of hydrophobic interaction chromatography and two-dimensional gel electrophoresis. Mass spectroscopy and peptide microsequencing revealed that p58/53 is identical to the insulin receptor tyrosine kinase substrate p58/53 (IRSp53). Whereas IRSp58/53 has no significant homology to β-dystroglycan other than the one span of peptides that confers its antibody cross-reactivity, its localization to the PSD newly implicates insulin signaling at synapses. Analysis of IRSp58/53 mass profiles, peptides, and mRNA indicated that IRSp58 and IRSp53 are the product of the same coding sequence. Immunolocalization showed that IRSp58/53 is expressed in the synapserich molecular layer of the cerebellum. Immunostaining of cultured hippocampal neurons showed that both IRSp58/53 and insulin receptor are highly concentrated at synapses. Like IRSp58/53, insulin receptors are a component of the PSD fraction. Together, these data suggest that the synapse is a specialized site for insulin signaling in the brain.

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41

Fourmy, Daniel. "Les recepteurs pancreatiques des peptides cck/gastrine du cobaye et du chien : etude de leur selectivite et caracterisation structurale." Toulouse 3, 1986. http://www.theses.fr/1986TOU30173.

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42

Crowley, John J. "Cholesterol and Phospholipid Modulation of BK[subscript Ca] Channel Activity and Ethanol Sensitivity: a dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/107.

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The large conductance Ca++-activated K+ channel (BKCa) regulates neuronal excitability through the efflux of K+, in response to membrane depolarization and increases in intracellular Ca++. The activity of the BKCa channel is increased by acute exposure to ethanol (EtOH), which is thought to underlie, in part, the influence of the drug on peptide hormone release from neurohypophysial nerve terminals (Dopico et al., 1996, 1998). Moreover, chronic EtOH exposure attenuates acute drug action on hormone release, and reduces the sensitivity of BKCa channels to acute EtOH exposure (Knott et al., 2002). The factors regulating EtOH action on BKCa channels are not well understood. Several lines of evidence suggest, however, that the lipid composition of the plasma membrane may influence channel sensitivity to the drug. The plasma membrane is highly complex in its organization (Welti and Glaser, 1994; Brown and London, 1998). There is a growing body of literature indicating that the local lipid composition of the membrane can influence the function of ion channels, including BKCa (Chang et al., 1995a, b; Moczydlowski et al., 1985; Park et al., 2003; Turnheim et al., 1999). Interestingly, chronic exposure to EtOH in animal models results in alterations in the composition of synaptic plasma membranes, including changes in the amount and distribution of membrane cholesterol (CHS) (Chin et al., 1978; Chin et al., 1979; Wood et al., 1989). The significance of these alterations is unclear. Here, we set out to determine the ability of membrane lipids to modulate BKCa channel activity and EtOH sensitivity. To address this, we implement the planar lipid bilayer technique, allowing control of both the protein and lipid components of the membrane. Native BKCa channels retain EtOH sensitivity in this reductionist preparation (Chu et al., 1998), and we extend the study here to examine cloned human brain (hslo) BKCachannels. We show here that hslo channels maintain their characteristic large conductance, voltage and Ca++-dependent gating, and sensitivity to 50 mM EtOH in bilayers cast from a 3:1 mixture of 1-pamiltoyl-2-oleoyl-phosphatidylethanolamine (POPE) and 1-pamiltoyl-2-oleoyl-phosphatidylserine (POPS). The addition of CHS to the bilayer decreases both the basal activity and EtOH sensitivity of the channels, in a concentration-dependent manner. This lends support to the notion that alterations in plasma membrane CHS levels following chronic EtOH exposure may reflect adaptations to the acute actions of the drug on ion channels. Furthermore, the EtOH sensitivity and CHS modulation of these reconstituted hslo channels are greatly reduced in the absence of negatively charged POPS in the bilayer (pure POPE). Based on these findings, we look to gain mechanistic insight into the lipid headgroup and acyl chain properties that may regulate BKCa channel modulation by EtOH and CHS. When POPS is replaced with the uncharged lipid 1-palmitoyl-2-oleoyl-phosphatidylcholine (POPC), the hslo response to EtOH and CHS is restored, suggesting that the loss of negative surface charge or PS headgroup structure itself cannot explain the lack of channel modulation by these agents in POPE bilayers. Moreover, increases in the proportion of unsaturated acyl chains in the bilayer cannot significantly influence the hslo response to EtOH. The loss of EtOH sensitivity in pure POPE and CHS-containing bilayers may, therefore, reflect the propensity of POPE and CHS to form nonlamellar (nonbilayer) structures. Regarding the basal activity of the channel, we demonstrate that decreases in negative surface charge, increases in the proportion of unsaturated acyl chains, and increases in the complexity of head group interactions can all influence the steady-state activity of reconstituted hslochannels, relative to control POPE/POPS (3:1) bilayers. Overall, these data further suggest the ability of the local lipid environment to regulate the basal function and EtOH sensitivity of an ion channel protein. Parts of this dissertation have appeared in separate publications: Treistman, S.N., O'Connell, R.J., and Crowley, J.J. (2002). Artificial Bilayer Techniques in Ion Channel Study. In Methods in Alcohol-Related Neuroscience Research, D. Lovinger and Y. Liu, eds. (Boca Raton, Florida: CRC Press) Crowley, J.J., Treistman, S.N., and Dopico, A.M. (2003). Cholesterol antagonizes ethanol potentiation of human BKCA channels in binary phospholipid bilayers. Mol. Pharma. 64(2):364-372.

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43

Yip, Rupert G. "Signal Transduction Mechanisms for the Stimulation of Lipolysis by Growth Hormone: A Dissertation." eScholarship@UMMS, 1994. https://escholarship.umassmed.edu/gsbs_diss/108.

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The purpose of this study was to investigate the mechanism of action of lipolysis by growth hormone in rat adipocytes. GH-induced lipolysis, in contrast to that of isoproterenol (ISO), is slow in onset (lag time >1h), small in magnitude (~2X basal). and requires corticosteroid. Evidence for direct coupling between GH receptors and adenylyl cyclase or G-proteins is lacking, and although we could detect no measurable change in cAMP content after treatment with GH + dexamethasone (Dex), it is likely that cAMP activation of protein kinase A is a central event in GH-induced lipolysis. Rp-cAMPS, a competitive antagonist of cAMP was equally effective in decreasing lipolysis in tissues treated with GH/Dex or a comparably lipolytic dose of ISO. Incorporation of 32P from γ-32P-ATP into kemptide, a synthetic oligopeptide substrate for protein kinase A, was increased in homogenates of GH/Dex-treated tissue. This increase was correlated with increased lipolysis. Earlier estimates based upon 32P-ribosylation of Gi catalysed by pertussis toxin (PTx) suggested that the abundance of Gi in adipocyte membranes was decreased 4h after treatment of hypophysectomized rats with GH. We therefore examined the possibility that changes in amount or distribution of G-proteins in adipocyte membranes might account for the lipolytic action of GH. Homogenates of GH/Dex-treated and control adipocytes were subjected to differential centrifugation and the abundance of G-proteins in low speed, l6k x g (16k), pellets and high speed, 100k x g (100k), pellets were determined by quantitative Western analysis with densitometry. A 35% loss of Giα2 from the l6k pellet compared from tissues treated with GH/Dex was associated with a 70% increase of Giα2 in the 100k pellet. No change in Gsα was observed in the l6k pellet but a 35% loss of Gsα was seen in the 100k pellet. The G proteins in the l6k pellet were fractionated on a continuous sucrose gradient followed by quantitation with Western analysis or autoradiography after 32P-NAD ribosylation. Giα2 was consistently shifted from heavier to lighter fractions of the l6k pellet after treatment with GH/Dex. Similar shifts of Gsα were not seen. The distribution of 32P-labelled proteins was comparably altered after incubation of homogenates of control and GH/Dex treated adipocytes with PTx and 32P-NAD. These shifts were blocked by treatment of adipocytes with 100μM colchicine which also blocked the lipolytic action of GH/Dex. We propose that an action of GH/Dex on the cytoskeleton of fat cells may change the cellular distribution of G-proteins in a manner that produces a relative decrease in the tonic inhibitory influence of Gi on adenylyl cyclase.

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44

Deb, Joyita. "Protein-hormone interactions patterning the gynoecium." Thesis, University of East Anglia, 2015. https://ueaeprints.uea.ac.uk/54301/.

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The gynoecium is among the most intricately patterned organs of the plant, comprisingdifferent tissue sub-structures, all with the purpose of facilitating propagation to the next generation. It is therefore representative of the complexity involved in the initiation and establishment of organ patterning and presents a unique model to study the mechanisms coordinating development. As with all other organs, the interplay between genetic and hormonal factors specifies carpel development. However, although much is known about the genetic components involved in carpel development, our understanding of hormonal regulation and the cross-talk between these two pathways is limited. Thus, the aim of this thesis has been to address this issue by obtaining an integrated view of the genetic and hormonal regulatory mechanisms which act to coordinate gynoecium development. It has done so using broadly two approaches: first, by characterising the transcription factor interactions which pattern the carpel, and second, by elucidating the cross-talk between these interactions and the plant hormone auxin. Further, it has also studied the role of auxin in carpel morphogenesis. Observations from this research have uncovered a novel auxin co-receptor complex formed by the transcription factors IND and ETT. The co-receptor binds the IAA molecule directly and exhibits specificity for IAA over the synthetic analogues NAA and 2,4-D. This coreceptor functions to coordinate the development of the style and stigmatic tissues of the carpel, possibly via the regulation of PID kinase. Further, this work has also identified novel roles in protein-protein dimerisation for the domains involved in this interaction. Analyses also indicate that this novel auxin signalling pathway may also be conserved in the Brassicaceae through the ETT orthologues in this family. Finally, this project has analysed how ETT’s role as an auxin receptor could be translated into precise spatiotemporal regulation of its target genes to specify the boundaries necessary for gynoecium patterning. Together, the results from this work have posed new questions as to the signalling mechanisms through which auxin coordinates its varied and numerous functions in plants.

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45

Du, Ling. "CIS/SOCS Proteins in Growth Hormone Action: A Dissertation." eScholarship@UMMS, 2000. https://escholarship.umassmed.edu/gsbs_diss/92.

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CIS/SOCS (cytokine-inducible SH2 protein/suppressor of cytokine signaling) are a family of proteins that are thought to act as negative regulators of signaling by erythropoetin, interleukin-6 and other cytokines whose receptors are related to the growth hormone receptor (GHR), and like growth hormone (GH), signal through the JAK/STAT pathway. We examined the possibility that CIS/SOCS proteins may also be involved in GH signaling, in particular, in termination of the transient insulin-like effects of GH. mRNAs for CIS, SOCS3, and to a lesser extent SOCS1 were detectable by Northern blot analysis of rat adipocyte total RNA, and the expression of CIS and SOCS3 was markedly increased 30 min after incubation with 500 ng/ml hGH. Both CIS and SOCS3 were detected in adipocyte extracts by immunoprecipitation and immunoblotting with their corresponding antisera. GH stimulated the tyrosine phosphorylation of a 120 kDa protein (p120) that was co-precipitated from adipocyte extracts along with αCIS and detected in Western blots with phospho-tyrosine antibodies. However, no tyrosine phosphorylated proteins in these cell extracts were immunoprecipitated with antibodies to CIS3/SOCS3. p120 was later identified as the GHR based on the observations that two GHR antibodies recognized p120 in scale-up experiments and that p120 and the GHR share several characteristics, including their molecular weights, tyrosine phosphorylation upon GH stimulation, interaction with CIS, similar extent of glycosylation as judged by electrophoretic mobility shift after Endo F digestion, comparable mobility shifts upon thrombin digestion, and N-terminal histidine-tagging. The findings, however, do not rule out the possibility that there might be other tyrosine phosphorylated 120 kDa protein(s) that interact with CIS and contribute to the p120 signal, as well as the GHR. Further studies of the association of CIS with the GHR revealed that CIS might selectively interact with multiply tyrosine phosphorylated forms of the GHR, and these tyrosines are likely located near the carboxyl end of the GHR. Overexpression of CIS partially inhibited GH-induced STAT5 phosphorylation in CHO cells. Studies in freshly isolated and GH-deprived (sensitive) adipocytes revealed that the abundance of CIS does not correlate with the termination of the insulin-like effects of GH or the emergence of refractoriness. Neither the association of CIS with the GHR nor the tyrosine phosphorylation status of the GHR, JAK2 and STAT5 appear responsible for refractoriness in adipocytes. These data imply that some negative regulators other than CIS might contribute to the termination of GH-induced insulin-like effects in adipocytes.

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46

BERTHELIER-BIHOREAU, CLAIRE. "Analyse des mecanismes de couplage dans l'antehypophyse : fonctions de la cascade arachidonique et des flux calciques." Paris 6, 1988. http://www.theses.fr/1988PA066078.

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47

Rico, Bautista Elizabeth. "Negative regulation of growth hormone (GH) signaling /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-184-9/.

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48

Oh, Seung Wook. "Regulation of Life Span by DAF-16/Forkhead Transcription Factor in Caenorhabditis elegans: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/22.

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The insulin/IGF-1 signaling pathway plays a pivotal role in life span regulation in diverse organisms. In Caenorhabditis elegans, a PI 3-kinase signaling cascade downstream of DAF-2, an ortholog of the mammalian insulin and insulin-like growth factor-1 (IGF-1) receptor, negatively regulates DAF-16/forkhead transcription factor. DAF-16 then regulates a wide variety of genes involved in longevity, stress response, metabolism and development. DAF-16 also receives signals from other pathways regulating life span and development. However, the precise mechanism by which DAF-16 directs multiple functions is poorly understood. First, in Chapter II, we demonstrate that JNK is a novel positive regulator of DAF-16 in both life span regulation and stress resistance. Our genetic analysis suggests that the JNK pathway acts in parallel with the insulin-like signaling pathway to regulate life span and both pathways converge onto DAF-16. We also show that JNK-1 directly interacts with and phosphorylates DAF-16. Moreover, in response to heat stress, JNK-1 promotes the translocation of DAF-16 into thc nucleus. Our findings define a novel interaction between the stress response pathway (JNK) and the master regulator of life span (DAF-16), and provide a mechanism by which JNK regulates longevity and stress resistance. Next, in Chapter III, we focus on the downstream targets of DAF-16. Here, we used a modified chromatin immunoprecipitation (ChIP) method to identify direct target promoters of DAF-16. We cloned 103 target sequences containing consensus DAF-16 binding sites and randomly selected 33 targets for further analysis. The expression of majority of these genes is regulated in a DAF-16-dependent manner. Moreover, inactivation of more than 50% of these genes significantly altered DAF-16-dependent functions such as longevity, fat storage and dauer diapause. Our results show that the ChIP-based cloning strategy leads to greater enrichment of DAF-16 target genes, compared to previous studies using DNA micro array or bioinformatics. We also demonstrate that DAF-16 is recruited to multiple promoters to coordinate regulation of its downstream target genes. In summary, we identified the JNK signaling pathway as a novel input into DAF-16 to adapt animals to the environmental stresses. We also revealed a large number of novel outputs of DAF-16. Taken together, these studies provide insight into the complex regulation by DAF-16 to control diverse biological functions and eventually broaden our understanding of aging.

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Prost, Edouard. "I : analyse structurale de la famille multigenique de l'hormone de croissance humaine. ii: etude de l'expression proteique du gene k10 implique dans le developpement dorso-ventral de l'oeuf de drosophile." Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR13136.

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50

Gardy-Godillot, Michèle. "Mise en evidence d'episodes secretoires du cortisol et de l'aldosterone au cours du nycthemere en relation avec les repas et certains acides amines de la ration." Clermont-Ferrand 2, 1988. http://www.theses.fr/1988CLF21112.

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Dissertations / Theses on the topic 'Hormone proteine'

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