Dissertations / Theses on the topic 'G-protein'
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Pateman, Cassandra Sophie Catherine. "RGS proteins and G protein signalling." Thesis, University of Warwick, 2002. http://wrap.warwick.ac.uk/2367/.
Full textMohr, Andrea. "Protein-Protein-Interaktionen des G-CSFR." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=960605398.
Full textHumrich, Jan. "G-Protein betagamma-Regulation durch Phosducin-like Proteine." kostenfrei, 2009. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2009/4005/.
Full textHiggs, C. "A computational study of the G-protein-G-protein coupled receptor interaction." Thesis, University of Essex, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324216.
Full textHowlett, Alyson Cerny. "Role of molecular chaperones in G protein B5-Regulator of G protein signaling dimer assembly and G protein By dimer specificity." BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2065.
Full textKong, Janice 1978. "G-protein coupled receptors (GPCRs) modulate regulator of G-protein signaling (RGS) selectivity." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33013.
Full textThe ability of RGSs to inhibit SSTR5 signaling was further assessed in cells expressing modified Gpa1 proteins.
Yeast have also been shown to be a useful model organism for the study of the localization of mammalian RGS proteins. We have constructed a series of vectors that allow us to express proteins fused to a Green Fluorescent Protein (GFP). (Abstract shortened by UMI.)
Fransen, Maikel Peter. "Stabilizing the G protein-coupled receptor rhodopsin/heterotrimeric G protein transducin signalling complex." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610816.
Full textGuillemot, Jean-Claude. "Contribution à l'étude des petites protéines -G." Toulouse 3, 1995. http://www.theses.fr/1995TOU30216.
Full textHowlett, Alyson Cerny. "Role of molecular chaperones in G protein "beta"5-regulator of G protein signaling dimer assembly and G protein "beta""gamma" specificity /." Diss., CLICK HERE for online access, 2009. http://contentdm.lib.byu.edu/ETD/image/etd2874.pdf.
Full textSheng, Yinglun. "G protein signaling and G protein coupled receptor (GPCR) pathway in Xenopus oocyte maturation." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/29262.
Full textBrockmann, Jörg. "Regulation G-Protein-gekoppelter Rezeptorkinasen." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=979675677.
Full textMarchese, Adriano. "Orphan G protein-coupled receptors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq41468.pdf.
Full textGhimire, Ganga D., ガンガ D. ギミレ, Kenichiro Imai, 賢一郎 今井, Fumitsugu Akazawa, 史嗣 赤沢, Toshiyuki Tsuji, et al. "Physicochemical properties of amino acid sequences of G-proteins for understanding GPCR-G-protein coupling." Chem-Bio Informatics Society, 2006. http://hdl.handle.net/2237/9277.
Full textGros, Robert. "Regulation of G-protein-coupled receptor function, a role for increased G-protein-coupled receptor kinase-2 protein content." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0019/NQ58133.pdf.
Full textKikkou, Tatsuhiko. "NMR structural analysis of G protein activation peptides derived from seven transmembrane G protein-coupled receptors." 京都大学 (Kyoto University), 2008. http://hdl.handle.net/2433/124071.
Full textLai, Chun Wan Jeffrey. "Mechanism of G Protein Beta-Gamma Assembly Mediated by Phosducin-Like Protein 1." BYU ScholarsArchive, 2011. https://scholarsarchive.byu.edu/etd/3190.
Full textGräler, Markus. "Der G-Protein-gekoppelte Rezeptor EDG6." [S.l. : s.n.], 2000. http://www.diss.fu-berlin.de/2001/6/index.html.
Full textKidley, N. J. "Modelling G protein-coupled receptor activation." Thesis, University of Essex, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402792.
Full textJa, William Wei-Hua Rees Douglas C. "Peptide modulators of G protein signaling /." Diss., Pasadena, Calif. : California Institute of Technology, 2005. http://resolver.caltech.edu/CaltechETD:etd-01032005-161114.
Full textYang, Zhao 1970. "Identification of a novel anti-apoptotic protein and characterization of mammalian regulators of G protein signaling (RGSs) in yeast." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111875.
Full textBased on the observation that human RGS1 causes yeast cell growth arrest, I therefore used RGS1 expressing yeast cells to screen a mouse T cell cDNA library in order to find potential interacting proteins. From the screen, I identified a mouse sphingomyelin synthase 1 (SMS1) cDNA. By using a series of different apoptotic stimuli, such as hydrogen peroxide, osmotic stress, exogenous ceramide and its precursors, high temperature etc., SMS1 expression was found to suppress cell growth arrest and prevent viability decline, indicating that SMS1 represents an anti-apoptotic protein that functions by decreasing the intracellular level of pro-apoptotic ceramide.
Gene analysis further indicated that the SMS1 gene consists of 16 exons spread over a 256kb portion of mouse chromosome 19. It is alternatively spliced to produce 4 different transcripts (SMS1alpha1, SMS1alpha2, SMS1beta and SMS1gamma) and encode 3 different proteins (SMS1alpha, SMS1beta and SMS1gamma). Notably, I found that SMS1beta protein does not interfere with SMS1alpha anti-apoptotic function, although both of these two proteins contain the protein-protein interaction domain, sterile alpha motif (SAM), at their N-terminus.
I also carried out a study to examine GPCR-RGS interactions using the yeast expression system. Our lab had noticed that there was an extra RGS5 related protein that was detected by western blot analysis in the protein extracts prepared from yeast and HEK293 cells expressing RGS5. The size of the band was approximately 2 times the molecular weight of RGS5, indicating the possibility that RGS5 forms a dimer. To further examine this hypothesis, I, therefore, performed a series of experiments, included yeast 2 hybrid assays, to demonstrate that RGS5 does interact with itself. This is the first report that RGS can form a dimer. The implications for this finding are discussed in detail.
Lauffer, Benjamin E. L. "Protein interactions mediating endocytic recycling of G protein-coupled receptors." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3339215.
Full textWalker, Karen Nicola. "Protein engineering and characterisation of an IgG-binding domain based upon protein G from Streptococcus group G." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296376.
Full textHan, Li. "G protein coupled receptor signaling to phospholipase D1 mediated by G12 type G proteins, LIM kinase and cofilin." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968929923.
Full textConti, Sofia Alessandra. "Monoclonal antibodies purification via Protein G and protein A affinity chromatography." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2021.
Find full textGata, Gabriel. "Regulated export of G-protein coupled receptors." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T066.
Full textThe largest family of membrane receptors is constituted by conserved seven-membrane domain spanning receptors, the G-protein coupled receptors (GPCRs). They are involved in numerous cell responses and diseases thus being a major drug target. Receptor function is determined by the amount of active receptors at the cell surface, which depends on various parameters, such as the biosynthetic rate, the export to the cell surface from internal stores, the endocytosis and post-transcriptional modifications (i.e. phosphorylation). Only recently, the importance of the regulated export has emerged, shedding new light on the physiological role of receptor retention, release, chaperoning and escorting. This work concerns the regulated export mechanisms of two members of the GPCRs family, the chemokine receptor 5 (CCR5) and the metabotropic receptor of the g amino butyric acid (GABAB). Whereas CCR5 is likely a homo-dimer of 2 identical protomers, GABAB is an obligatory hetero-dimer of 2 distinct subunit known as GB1 and GB2. Both CCR5 and GB1 are retained in intracellular compartments (the ER and the Golgi) from which they are released in response to external signals (CCR5) and/or interaction with “private escort proteins” (CD4 for CCR5 and GB2 for GB1). The main goal of our work was to understand the mechanism of retention of these receptors and its regulation. In this context, we determined using biochemical and biophysical approaches that these GPCRs specifically interact with the members of the Prenylated Rab Acceptor Family (PRAF). These proteins are resident either in the ER (PRAF2 and PRAF3) or in the Golgi apparatus (PRAF1) where they function as receptor gatekeepers. Indeed, we could document for PRAF2 that this protein likely interacts directly with previously identified receptor retention motifs and inhibits receptor egress from the ER and subsequent trafficking to the plasma membrane. In the context of the GABAB receptor, PRAF2-dependent retention of GB1 can be overridden by GB2 via simple competition. Perturbing the stoichiometry of PRAF gatekeepers respective to that of receptors significantly perturbs receptor function both in vitro and in vivo. Because PRAFs are ubiquitous and seem to interact with many other GPCRs, they might represent major regulators of receptor function both in physiological and pathological conditions
Dasso, Leonardo. "Receptor-G protein interactions in rat hepatocytes." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282114.
Full textWhite, Colin D. "Dissection of GnRH receptor-G protein coupling." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3885.
Full textTaddese, Bruck. "Computational modelling of G protein-coupled receptors." Thesis, University of Essex, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589439.
Full textHo, H. M. I. "Regulation of G protein-gated K+channels." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604105.
Full textGibson, W. T. "G-protein signalling pathways and appetite regulation." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599391.
Full textSun, Xianqiang. "Theoretical Studies of G-Protein-Coupled Receptors." Doctoral thesis, KTH, Teoretisk kemi och biologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-166407.
Full textQC 201505020
Henne, Randal Marlow. "Computational studies of G-protein coupled receptors /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8048.
Full textSlessareva, Janna Eugenievna. "Molecular mechanisms of G protein-receptor coupling." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2907.
Full textTitle from document title page. Document formatted into pages; contains vi, 200 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
Ma, Hongzheng. "Molecular mechanisms of G protein-receptor coupling." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2978.
Full textTitle from document title page. Document formatted into pages; contains viii, 264 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
Zazzu, Valeria. "The human G protein-coupled receptor GPR30." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16325.
Full textIn 1997, the orphan G protein-coupled receptor 30, GPR30, was cloned using HUVECs exposed to FSS. It was shown that the level of GPR30 expression was up-regulated in response to FSS. Subsequently, in a study performed in the laboratory where the work for this thesis was carried out, the cellular and tissue distribution of GPR30 were investigated in GPR30-LacZ reporter mice and the expression was found predominantly in the endothelial cells of small arteries in several tissue types. GPR30, was also claimed to bind 17-β-estradiol (E2) directly and to mediate rapid non-genomic signalling. In contrast, various reports have indicated that E2 fails to bind GPR30 in a specific manner. Despite the controversy on whether GPR30 is an estrogen receptor or not, nothing is known at present about its relation and interaction with other proteins. Therefore, the aim of the work described in this thesis was to identify human GPR30 protein interaction partners and to establish a human vascular in vitro model in order to evaluate the potential role of GPR30 and the downstream effects of the interaction between GPR30 and new interaction partners in a vascular model at transcript level. The screening of a human heart cDNA library using the yeast two-hybrid assay led to the identification of several interaction partners for GPR30, among them PATJ and FUNDC2. These interactions were verified by CoIP experiments and the interaction of GPR30 with PATJ could be confirmed. The effect of FSS on the expression of GPR30 was confirmed in HUVECs and was detected in other endothelial cell types. In HUAECs, HAoECs and HMEC-1 cells GPR30 was also found up-regulated upon FSS, suggesting that GPR30 may indeed play a key role in vascular physiology. Finally, the role of GPR30 and PATJ in the FSS response was investigated at the genome-wide transcript level in HMEC-1 cells. Interestingly, a different panel of genes was deregulated owing to FSS in cells over-expressing GPR30 compared to FSS alone.
Rose, Alexander. "The dynamic coupling interface of G-protein coupled receptors." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17215.
Full textTo communicate with their environment, living cells feature receptors that provide a bridge across the enclosing membrane. The prevalent G protein-coupled receptors (GPCR) receive outside information through the binding of a ligand, which activates the receptor. During activation, an open intracellular crevice forms, to which a G protein (Gαβγ, G) can couple with its Gα C-terminus. Binding to GPCRs triggers GDP/GTP exchange in the Gα subunit of Gαβγ, necessary for further signal transfer within the cell. The coupling between receptor and Gαβγ involves a series of dynamic structural changes that govern speed and specificity of the interaction. Here we used molecular dynamics (MD) simulations to elucidate molecular details of the GPCR Gαβγ coupling process before and during GPCR Gαβγ complex formation up to the GDP/GTP exchange.
Hill, Claire Louise. "The use of Schizosaccharomyces pombe to investigate reguator of G protein signalling proteins." Thesis, University of Warwick, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487827.
Full textBarclay, Elaine. "Characterisation of palmitoylation in alpha₂_A adrenoceptor and 5-HT₁_A serotonin receptor-G₀₁α G protein fusion proteins." Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4998/.
Full textSagi, Sarah Ann. "G alpha q- and G alpha 12-mediated signaling pathways activated by G protein-coupled thrombin receptors /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9992384.
Full textLo, Kin Ho. "Activation of signal transducer and activator of transcription 3 (STAT3) by G[alpha]16 and G[alpha]14 via a c-Src/JAK-and ERK-dependent mechanism /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BICH%202004%20LO.
Full textIncludes bibliographical references (leaves 92-111). Also available in electronic version. Access restricted to campus users.
Ip, Koon-ching. "Role of G[alpha]-interacting protein (GAIP) in modulation of MAPK pathways /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20IP.
Full textRunne, Caitlin M. "Function and Activation Mechanism of PLEKHG2, A Novel G Beta Gamma-Activated RhoGEF in Leukemia Cells." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/4907.
Full textKumas, Gozde. "Detecting G-protein Coupled Receptor Interactions Using Enhanced Green Fluorescent Protein Reassembly." Master's thesis, METU, 2012. http://etd.lib.metu.edu.tr/upload/12614136/index.pdf.
Full textis an innovative approach based on the reassembly of protein fragments which directly report interactions. In our study we implemented this technique for detecting and visualizing the GPCR interactions in yeast cells. The enhanced green fluorescent protein (EGFP) fractionated into two fragments at genetic level which does not possess fluorescent function. The target proteins which are going to be tested in terms of interaction are modified with the non-functional fragments, to produce the fusion proteins. The interaction between two target proteins, in this study Ste2p receptors which are alpha pheromone receptors from Saccharomyces cerevisiae, enable the fragments to come in a close proximity and reassemble. After reassembly, EGFP regains its fluorescent function which provides a direct read-out for the detection of interaction. Further studies are required to determine subcellular localization of the interaction. Moreover, by using the fusion protein partners constructed in this study, effects of agonist/antagonist binding and post-translational modifications such as glycosylation and phosphorylation can be examined. Apart from all, optimized conditions for BiFC technique will guide for revealing new protein-protein interactions.
Gaudio, Sabrina. "Functional characterization of the interaction between G protein coupled receptors (GPCR) and regulators of G protein signaling (RGS) in yeast." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97959.
Full textStewart, Adele Marie. "Regulator of G protein signaling 6 (RGS6), a multifarious and pleiotropic modulator of G protein coupled receptor signaling in brain." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/4765.
Full textTeichmann, Anke. "Fluoreszenzmikroskopische Untersuchungen zur Interaktion G-Protein gekoppelter Rezeptoren." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16671.
Full textThe heptahelical G protein-coupled receptors (GPCRs) are important drug targets. Following activation by their ligands, they exert their function via the binding of G proteins and activation of specific signal transduction cascades. To date, the functional significance of the oligomerization of GPCRs is not completely understood. For some GPCRs it could be shown that the oligomerization modulates receptor transport and/or the dynamics of receptor activation. Most importantly, it is not clear whether the GPCRs exist exclusively as oligomers or in a certain monomer-dimer ratio (M/D) or whether a given ratio is dynamic. In this work, the homo-oligomerization of the endothelin-B-receptor (ETBR), the vasopressin-V2-receptor (V2R) and the corticotropin-releasing-factor-receptors type 1 (CRF1R) and type 2(a) (CRF2(a)R) was analysed. In addition, the M/D of these GPCRs was determined. For the detection of the protein-protein interactions, the following biophysical methods were established: fluorescence-resonance-energy-transfer (FRET) and fluorescence-crosscorrelation-spectroscopy (FCCS). With the help of FCCS, a specific M/D could be determined for each of the GPCRs. Using FRET, differences in the interaction dynamics between family 1 (V2R) and family 2 GPCRs (CRF1R) could be described. Moreover, it was experimentally verified that the CRF2(a)R is exclusively expressed as a monomer, in contrast to the other GPCRs and even the highly homologous CRF1R. Using signal peptide swap experiments, it could be demonstrated that the N-terminal pseudo signal peptide of the CRF2(a)R, which is so far unique in the superfamily of GPCRs, prevents oligomerization of the receptor. In addition, a relation of receptor oligomerization and G protein coupling selectivity was established for the CRF1R and the CRF2(a)R which is novel for the GPCR protein family.
Zheng, Bin. "RGS proteins : bridging the "GAP"s between G protein signaling and membrane trafficking /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2002. http://wwwlib.umi.com/cr/ucsd/fullcit?p3059905.
Full textBurger, Katja. "Cholesterin und Progesteron - Modulatoren G-Protein-gekoppelter Signaltransduktionswege." [S.l.] : [s.n.], 2000. http://ArchiMeD.uni-mainz.de/pub/2001/0031/diss.pdf.
Full textSchnelzer, Andreas Christof. "Untersuchungen zum kleinen G-Protein Rac1 beim Mammakarzinom." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963997610.
Full textRitscher, Lars. "Die Agonistspezifität des G-Protein-gekoppelten Rezeptors GPR34." Doctoral thesis, Universitätsbibliothek Leipzig, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-97551.
Full textLyso-PS (lyso-phosphatidylserine) has been shown to activate the G(i/o)-protein-coupled receptor GPR34. Since in vitro and in vivo studies provided controversial results in assigning lyso-PS as the endogenous agonist for GPR34, we investigated the evolutionary conservation of agonist specificity in more detail. Except for some fish GPR34 subtypes, lyso-PS has no or very weak agonistic activity at most vertebrate GPR34 orthologues investigated. Using chimaeras we identified single positions in the second extracellular loop and the transmembrane helix 5 of carp subtype 2a that, if transferred to the human orthologue, enabled lyso-PS to activate the human GPR34. Significant improvement of agonist efficacy by changing only a few positions strongly argues against the hypothesis that nature optimized GPR34 as the receptor for lyso-PS. Phylogenetic analysis revealed several positions in some fish GPR34 orthologues which are under positive selection. These structural changes may indicate functional specification of these orthologues which can explain the species- and subtype-specific pharmacology of lyso-PS. Furthermore, we identified aminoethyl-carbamoyl ATP as an antagonist of carp GPR34, indicating ligand promiscuity with non-lipid compounds. The results of the present study suggest that lyso-PS has only a random agonistic activity at some GPR34 orthologues and the search for the endogenous agonist should consider additional chemical entities