Relevant bibliographies by topics / G-protein

Academic literature on the topic 'G-protein'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "G-protein"

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Iyengar, R. "Structure of G Protein-Coupled Receptors and G Proteins." Science Signaling 2005, no. 276 (March 18, 2005): tr10. http://dx.doi.org/10.1126/stke.2762005tr10.

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Andreeva, Alexandra V., Mikhail A. Kutuzov, and Tatyana A. Voyno- Yasenetskaya. "Scaffolding proteins in G-protein signaling." Journal of Molecular Signaling 2 (October 30, 2007): 13. http://dx.doi.org/10.1186/1750-2187-2-13.

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Santagata, S. "G-Protein Signaling Through Tubby Proteins." Science 292, no. 5524 (May 24, 2001): 2041–50. http://dx.doi.org/10.1126/science.1061233.

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Spiegel, Allen M., and Lee S. Weinstein. "Inherited Diseases Involving G Proteins and G Protein–Coupled Receptors." Annual Review of Medicine 55, no. 1 (February 2004): 27–39. http://dx.doi.org/10.1146/annurev.med.55.091902.103843.

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Campbell, Adrian P., and Alan V. Smrcka. "Targeting G protein-coupled receptor signalling by blocking G proteins." Nature Reviews Drug Discovery 17, no. 11 (September 28, 2018): 789–803. http://dx.doi.org/10.1038/nrd.2018.135.

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Morikawa, T., T. Ishii, A. Arai, T. Kohno, K. Sato, Y. Kato, M. Tanokura, and K. Wakamatsu. "Interaction of G protein with G protein activating peptides." Seibutsu Butsuri 43, supplement (2003): S181. http://dx.doi.org/10.2142/biophys.43.s181_1.

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Oldham, William M., and Heidi E. Hamm. "Heterotrimeric G protein activation by G-protein-coupled receptors." Nature Reviews Molecular Cell Biology 9, no. 1 (January 2008): 60–71. http://dx.doi.org/10.1038/nrm2299.

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Heuss, Christian, and Urs Gerber. "G-protein-independent signaling by G-protein-coupled receptors." Trends in Neurosciences 23, no. 10 (October 2000): 469–75. http://dx.doi.org/10.1016/s0166-2236(00)01643-x.

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Blumer, Joe B., and Stephen M. Lanier. "Accessory Proteins for G Protein-Signaling Systems: Activators of G Protein Signaling and Other Nonreceptor Proteins Influencing the Activation State of G Proteins." Receptors and Channels 9, no. 3 (January 2003): 195–204. http://dx.doi.org/10.3109/10606820308240.

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Blumer, Joe B., and Stephen M. Lanier. "Accessory Proteins for G Protein-Signaling Systems: Activators of G Protein Signaling and Other Nonreceptor Proteins Influencing the Activation State of G Proteins." Receptors and Channels 9, no. 3 (May 1, 2003): 195–204. http://dx.doi.org/10.1080/10606820308240.

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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/.

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The work within this thesis is concerned with the creation of a temperature-sensitive Schizosaccharomyces pombe marker protein, and the regulation of the pheromone communication system of Sz. pombe reporter strains by RGS proteins. There are a limited number of marker proteins available for use in the genetic manipulation of Sz. pombe, and the generation of a temperature-sensitive Ura4p was envisaged to expand the scope of carrying out sequential gene disruptions in the fission yeast. PCR-based mutagenesis was used to introduce mutations in the ura4 cassette, and a leucine to proline mutation identified at residue 261 in the ura4 open reading frame conferred a temperature-sensitive requirement for uracil. To demonstrate the use of the Ura4sp marker in gene disruption, the Sz. pombe irpl gene was disrupted with the ura4u cassette, and subsequently, the prkl gene was disrupted with the wild-type ura4 cassette. RGS proteins are a recently discovered family of proteins that negatively regulate G protein-coupled signalling pathways. This thesis describes the ability of mammalian RGS proteins to regulate the pheromone communication system of Sz. pombe reporter strains. Human RGS 1 and human RGS4 displayed the greatest ability to negatively regulate the Sz. pombe pheromone signalling pathway when expressed from multicopy expression vectors. Human RGS2, human RGS3, human RGS9-2 and murine RGS2 displayed lesser, varying abilities. Expression of human RGS 1 from single copy reduced signalling at low pheromone concentrations. Expression of human RGS4 from single copy was incapable of reducing pheromone-independent and pheromone-dependent signalling. This thesis also describes the search for gain-of-function RGS proteins. Two potential gain-of-function szRgslp mutants were previously identified, and these mutants were recreated. The two mutations identified (histidine to arginine at szRgslp residue 171 and valine to isoleucine at szRgslp residue 305) conferred gain-of-function szRgslp phenotypes in an sxa2:: ura4 reporter strain. Hydroxylamine treatment of the human RGS4 open reading frame resulted in the identification of a potential gain-of-function RGS4 mutant. The lysine to arginine mutation at huRGS4p residue 20 conferred a gain-of-function huRGS4p phenotype in an sxa2:: ura4 reporter strain.
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Mohr, Andrea. "Protein-Protein-Interaktionen des G-CSFR." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=960605398.

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Humrich, Jan. "G-Protein betagamma-Regulation durch Phosducin-like Proteine." kostenfrei, 2009. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2009/4005/.

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Higgs, 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.

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Howlett, 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.

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In order for G protein signaling to occur, the G protein heterotrimer must be assembled from its nascent polypeptides. The most difficult step in this process is the formation of the Gβγ dimer from the free subunits since both are unstable in the absence of the other. Recent studies have shown that phosducin-like protein (PhLP1) works as a co-chaperone with the cytosolic chaperonin complex (CCT) to fold Gβ and mediate its interaction with Gγ. However, these studies did not address questions concerning the scope of PhLP1 and CCT-mediated Gβγ assembly, which are important questions given that there are four Gβs that form various dimers with 12 Gγs and a 5th Gβ that dimerizes with the four regulator of G protein signaling (RGS) proteins of the R7 family. The data presented in Chapter 2 shows that PhLP1 plays a vital role in the assembly of Gγ2 with all four Gβ1-4 subunits and in the assembly of Gβ2 with all twelve Gγ subunits, without affecting the specificity of the Gβγ interactions. The results of Chapter 3 show that Gβ5-RGS7 assembly is dependent on CCT and PhLP1, but the apparent mechanism is different from that of Gβγ. PhLP1 seems to stabilize the interaction of Gβ5 with CCT until Gβ5 is folded, after which it is released to allow Gβ5 to interact with RGS7. These findings point to a general role for PhLP1 in the assembly of all Gβγ combinations, and suggest a CCT-dependent mechanism for Gβ5-RGS7 assembly that utilizes the co-chaperone activity of PhLP1 in a unique way. Chapter 4 discusses PhLP2, a recently discovered essential protein, and member of the Pdc family that does not play a role in G protein signaling. Several studies have indicated that PhLP2 acts as a co-chaperone with CCT in the folding of actin, tubulin, and several cell cycle and pro-apoptotic proteins. In a proteomics screen for PhLP2A interacting partners, α-tubulin, 14-3-3, elongation factor 1α, and ribosomal protein L3 were found. Further proteomics studies indicated that PhLP2A is a phosphoprotein that is phosphorylated by CK2 at threonines 47 and 52.
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Kong, 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.

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Regulators of G-protein Signaling (RGSs) are negative regulators of G-protein Coupled Receptor (GPCR) mediated signaling that function to limit the lifetime of receptor-activated Galpha proteins. Heterologously expressed mammalian RGSs can functionally complement a yeast mutant lacking its RGS containing gene SST2. Here we show that four mammalian RGSs differentially inhibit the activation of a FUS1-LacZ reporter gene by the STE2 encoded GPCR in yeast with the apparent rank order potency: RGS1 > RGS16 > RGS2 > RGS5. In order to examine the role of the GPCR in modulating RGS function, we functionally expressed the human somatostatin receptor 5 (SSTR5) in yeast.
The 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.)
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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.

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Guillemot, Jean-Claude. "Contribution à l'étude des petites protéines -G." Toulouse 3, 1995. http://www.theses.fr/1995TOU30216.

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L'adnc humain de d4-gdi a ete clone au laboratoire par soustraction de banque d'adnc entre lignees hematopoietiques et non hematopoietiques. Au niveau acides amines, ce gene montre une homologie de 68% avec rho-gdi, inhibiteur de la dissociation du gdp pour rho. La famille des proteines ras, les petites proteines g, se comporte de plusieurs sous-groupes: ras/raf, rab, tc4/ran et rho. L'analyse par northern du profil d'expression de d4-gdi nous a montre qu'il est exprime preferentiellement dans les cellules hematopoietiques. Afin d'etudier ce gene, nous en avons etabli une mutation nulle par recombinaison homologue dans des cellules embryonnaires souches de souris. Plusieurs laboratoires, dont le notre, ont decrit la possibilite d'obtenir une differenciation hematopoietique in vitro a partir de cellules es. Nous avons ainsi montre que d4-gdi n'est pas implique dans l'hematopoiese
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Howlett, 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.

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Sheng, 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.

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Xenopus laevis oocytes are physiologically arrested at the first meiotic prophase. Progesterone reinitiates meiosis (maturation) through inhibition of an oocyte adenylyl cyclase (AC) and reduction of intracellular cAMP. However, the mechanism by which progesterone regulates AC activity and cAMP level still remains unclear. In this thesis, I summarize work I conducted that collectively helps elucidate how high levels of cAMP might be achieved in G2 arrested oocytes. In Chapter 2, I describe our finding that inhibiting endogenous G-protein betagamma subunits, through the use of two structurally distinct Gbetagamma scavengers, causes hormone-independent oocyte maturation. In contrast, overexpression of Xenopus Gbeta1, alone or together with bovine Ggamma2, inhibits progesterone-induced oocyte maturation. These results for the first time implicate that an endogenous G protein coupled receptor system releases a Gbetagamma complex as the dominant meiosis inhibitor. Chapter 3 describes my research aiming to reveal the identity of the oocyte AC responsible for generating meiosis-inhibiting cAMP. I provide further evidence here that the ability of Gbetagamma to inhibit meiosis is attributed to the activation of an endogenous AC, rather than other possible Gbetagamma effectors. Through molecular cloning and biochemical characterization, I discovered that the likely AC candidate is Xenopus AC7, an isoform that is activated by Gbetagamma, but only in the presence of GTP-bound Gsalpha. The identification of xAC7 suggests that the maintenance of high levels of cAMP may require the cooperation of Gsalpha and Gbetagamma. Finally, in Chapter 4, I describe our efforts in identifying the GPCR(s) responsible for activating the cAMP signaling in prophase-arrested oocytes. A screening of known antagonists of GPCR(s) led to the identification of ritanserin, a potent antagonist of serotonin receptors, as a potent maturation inducer in Xenopus oocytes. Pharmacological and molecular studies, however, have ruled out the involvement of a known serotonin receptor in meiosis arrest. Instead, the most likely candidate is a "constitutively activated" GPCR that bears structural similarities to Xenopus serotonin receptor 7.
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Books on the topic "G-protein"

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Smrcka, Alan V. G Protein Signaling. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592594301.

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Ravi, Iyengar, and Hildebrandt John D, eds. G protein pathways. San Diego: Academic Press, 2002.

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Ravi, Iyengar, and Hildebrandt John D, eds. G protein pathways. San Diego: Academic Press, 2002.

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R, George Susan, and O'Dowd Brian Francis 1950-, eds. G protein-coupled receptor-protein interactions. Hoboken, N.J: Wiley-Liss, 2005.

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J, Biden Trevor, and Shine John, eds. G protein-coupled receptors. New York: Springer-Verlag, 1995.

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Poyner, David R., and Mark Wheatley, eds. G Protein-Coupled Receptors. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9780470749210.

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Siehler, Sandra, and Graeme Milligan, eds. G Protein-Coupled Receptors. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511760334.

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Giraldo, Jesus, and Jean-Philippe Pin, eds. G Protein-Coupled Receptors. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733441.

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Iismaa, Tiina P., Trevor J. Biden, and John Shine. G Protein-Coupled Receptors. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-21930-0.

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J, Peroutka Stephen, ed. G protein-coupled receptors. Boca Raton: CRC Press, 1994.

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Book chapters on the topic "G-protein"

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Colao, Annamaria, and Claudia Pivonello. "G Protein." In Encyclopedia of Pathology, 1–3. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5107-1.

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Colao, Annamaria, and Claudia Pivonello. "G Protein." In Endocrine Pathology, 283–85. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5107.

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Shetzline, Michael A., and Marc G. Caron. "G Proteins and G Protein-Coupled Receptors." In Hormone Signaling, 181–97. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_9.

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Nederkoorn, Paul H. J., Henk Timmerman, and Gabriëlle M. Donné-Op den Kelder. "G Protein-Coupled Receptors and G Proteins." In Signal Transduction by G Protein-Coupled Receptors, 43–62. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4684-1407-3_4.

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Ulloa-Aguirre, Alfredo, and P. Michael Conn. "G Protein-Coupled Receptors and G Proteins." In Principles of Molecular Regulation, 3–25. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-032-2_1.

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Wedegaertner, Philip B. "G Protein Trafficking." In Subcellular Biochemistry, 193–223. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4765-4_11.

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Bourne, Henry R. "G Protein Oncogenes." In Cellular Regulation by Protein Phosphorylation, 253–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75142-4_31.

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Falkenburger, Björn H. "G-Protein αq." In Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_351-1.

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, Ching-Kang Chen, Denis J. Dupré, Terence E. Hébert, Joe B. Blumer, et al. "G Protein Beta." In Encyclopedia of Signaling Molecules, 702. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100507.

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, Ching-Kang Chen, Denis J. Dupré, Terence E. Hébert, Joe B. Blumer, et al. "G Protein Gamma." In Encyclopedia of Signaling Molecules, 710. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100508.

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Conference papers on the topic "G-protein"

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Burke, John E., Alison J. Inglis, Oscar Vadas, Olga Perisic, Glenn R. Masson, Stephen H. McLaughlin, and Roger L. Williams. "Abstract IA02: G-proteins regulating PI3Ks and PI4KIIIβ regulating a G-protein." In Abstracts: AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; September 14-17, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.pi3k14-ia02.

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Mannes, Morgane, Charlotte Martin, Sarah Triest, Toon Laeremens, Christel J. Menet, and Steven Ballet. "Development of G Protein Peptidomimetics to Stabilize Active State G Protein-Coupled Receptors." In 36th European Peptide Symposium. The European Peptide Society, 2022. http://dx.doi.org/10.17952/36eps/36eps.2022.025.

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Li, Yonghui, Shan Hong, and Yanting Shen. "Enhancing pea protein functionalities through "green" modifications for food applications." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/dpor5716.

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Pea protein is receiving significant interest. Modified pea proteins may be used as healthy and more functional ingredients in food products. This study aimed to enhance pea protein functional properties through neoglycosylation with guar gum or gum arabic and/or enzymatic modification with transglutaminase or protein glutaminase, understand the physicochemical properties of the modified proteins, and evaluate their applications in mayonnaise-like dressings as egg replacers and in beef patties as functional extenders. The proteins crosslinked with transglutaminase showed significantly improved water holding capacity (5.2 - 5.6 g/g protein) compared with the control pea protein isolate (2.8 g/g). The pea proteins conjugated with guar gum showed exceptional emulsifying capacity (EC) and stability (ES) of up to 100% compared with the control protein (EC of 58% and ES of 48%). Some sequentially modified pea proteins, such as transglutaminase crosslinking followed by guar gum conjugation had multiple functional enhancements (water holding, oil holding, emulsifying, and gelation). The functionally enhanced pea proteins had comparable descriptive sensory scores as the control protein. Beef patties containing 2.5-5% of the modified pea protein from sequential deamidation and conjugation demonstrated some advantageous features in terms of higher fat/water retention, cooking yield, and tender texture, which may be preferred by the elderly or some other consumers. The emulsions with the guar gum conjugated protein had significantly increased stability, apparent viscosity, and decreased droplet size, and mayonnaise-like dressing prepared with this protein at higher concentrations (6 and 8%) exhibited significantly better emulsification properties and viscoelasticity, compared with those containing the unmodified protein.
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Fang, Ye, Anthony G. Frutos, and Joydeep Lahiri. "G protein-coupled receptor (GPCR) microarrays." In International Symposium on Biomedical Optics, edited by Darryl J. Bornhop, David A. Dunn, Raymond P. Mariella, Jr., Catherine J. Murphy, Dan V. Nicolau, Shuming Nie, Michelle Palmer, and Ramesh Raghavachari. SPIE, 2002. http://dx.doi.org/10.1117/12.472073.

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Brass, L. F., D. R. Manning, and M. J. Woolkalis. "G PROTEIN REGULATORS OF PHOSPHOLIPASE C AND ADENYLATE CYCLASE IN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644630.

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The hydrolysis of polyphosphoinositides (PI) by phospholipase C during platelet activation produces two key intracellular messengers, inositol triphosphate and diacylglycerol. This process is thought to be regulated by a guanine nucleotide binding protein referred to as Gp. Although the evidence that Gp exists is compelling, to date it has not been isolated. Uncertainty about its identity has been compounded by variations between tissues in the susceptibility of Gp to pertussis toxin and by reconstitution studies which show that pertussis toxin-inhibited PI hydrolysis can be restored by purified Gi, the pertussis toxin-sensitive G protein which inhibits adenylate cyclase. Therefore, it remains unclear whether Gp represents a new G protein or a second role for Gj. When platelets permeabilized with saponin were incubated with pertussis toxin and 32P-NAD, a single 42 kDa protein was 32P-ADP-ribosylated which co-migrated with the purified a subunit of Gi. Preincubating the platelets with an agonist inhibited labeling of this protein by dissociating the G protein into subunits. The extent of inhibition correlated with the number of toxin-sensitive functions caused by the agonist. Labeling was abolished by thrombin, which inhibited cAMP formation and caused toxin-inhibitable PI hydrolysis. Labeling was partially inhibited by vasopressin and platelet activating factor, which caused toxin-inhibitable PI hydrolysis, but had no effect on cAMP formation and by epinephrine, which inhibited cAMP formation, but did not cause PI hydrolysis. Labeling was unaffected by the TxA2 analog U46619, which neither caused toxin-sensitive PI hydrolysis nor inhibited cAMP formation. These observations suggest that the 42 kDa band may contain a subunits from both Gp and Gi and, in fact, 2D electrophoresis resolved the 42 kDa protein band into two proteins with distinct pi. However, those agonists linked functionally only to Gp or only to Gi decreased the labeling of both proteins. Therefore, our data suggest (1) that Gj and Gp are the same protein and (2) that whether a aiven platelet agonist affects adenylate cyclase or phospholipase C or both depends upon factors extrinsic to the G protein.
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"Protein-lipid nanoparticles for studying G-protein coupled receptors functional properties." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-146.

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Howl, John. "Chimeric ligands for G-protein-coupled receptors." In VIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 1999. http://dx.doi.org/10.1135/css199903009.

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Jakobs, K. H., P. Gierschik, and R. Grandt. "THE ROLE OF GTP-BINDING PROTEINS EXHIBITING GTPase ACTIVITY IN PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644773.

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Activation of platelets by agonists acting via cell surface-located receptors apparently involves as an early event in transmembrane signalling an interaction of the agonist-occupied receptor with a guanine nucleotide-binding regulatory protein (G-protein). The activated G-protein, then, transduces the information to the effector molecule, being responsible for the changes in intracellular second messengers. At least two changes in intracellular signal molecules are often found to be associated with platelet activation by agonists, i.e., increases in inositol trisphosphate and diacylglycerol levels caused by activation of a polyphosphoinositide-specific phospholipase C and decrease in cyclic AMP concentration caused by inhibition of adenylate cyclase.Both actions of platelet-activating agents apparently involve G-proteins as transducing elements. Generally, the function of a G-protein in signal transduction can be measured either by its ability to regulate the activity of the effector molecule (phospholipase C or adenylate cyclase) or the binding affinity of an agonist to its specific receptor or by the abitlity of the G-protein to bind and hydrolyze GTP or one of its analogs in response to agonist-activated receptors. Some platelet-activating agonists (e.g. thrombin) can cause both adenylate cyclase inhibition and phospholipase C activation, whereas others induce either inhibition of adenylate cyclase (e.g. α2-adrenoceptor agonists) or activation of phospholipase C (e.g. stable endoperoxide analogs) . It is not yet known whether the simultaneous activation of two signal transduction systems is due to activation of two separate G-proteins by one receptor, to two distinct receptors activating each a distinct G-protein or to activation of two effector molecules by one G-protein.For some of the G-proteins, rather specific compounds are available causing inactivation of their function. In comparison to Gs, the stimulatory G-protein of the adenylate cyclase system, the adenylate cyclase inhibitory Gi-protein is rather specifically inactivated by ADP-ribosylation of its a-subunit by pertussis toxin, “unfortunately” not acting in intact platelets, and by SH-group reactive agents such as N-ethylmaleimide and diamide, apparently also affecting the Giα-subunit. Both of these treatments completely block α2-adrenoceptor-induced GTPase stimulation and adenylate cyclase inhibition and also thrombin-induced inhibition of adenylate cyclase. In order to know whether the G-protein coupling receptors to phospholipase C is similar to or different from the Gi-protein, high affinity GTPase stimulation by agents known to activate phospholipase C was evaluated in platelet membranes. The data obtained indicated that GTPase stimulation by agents causing both adenylate cyclase inhibition and phospholipase C activation is reduced, but only partially, by the above mentioned Gi-inactivating agents, while stimulation of GTPase by agents stimulating only phospholipase C is not affected by these treatments. These data suggested that the G-protein regulating phospholipase C activity in platelet membranes is different from the Gi-protein and may also not be a substrate for pertussis toxin. Measuring thrombin stimulation of inositol phosphate and diacylglycerol formation in saponin-permeabilized platelets, apparently contradictory data were reported after pertussis toxin treatment, being without effect or causing even an increase in thrombin stimulation of inositol phosphate formation (Lapetina: BBA 884, 219, 1986) or being inhibitory to thrombin stimulation of diacylglycerol formation (Brass et al.: JBC 261, 16838, 1986). These data indicate that the nature of the phospholipase C-related G-protein(s) is not yet defined and that their elucidation requires more specific tools as well as purification and reconstitution experiments. Preliminary data suggest that some antibiotics may serve as useful tools to characterize the phospho-lipase-related G-proteins. The possible role of G-protein phosphorylation by intracellular signal molecule-activated protein kinases in attenuation of signal transduction in platelets will be discussed.
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Leite Nobrega De Moura Bell, Juliana. "Understanding the impact of proteolysis on extractability, physicochemical, and functional properties of proteins and lipids from almond flour." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/pyui3979.

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The extraction of lipids and proteins from food matrices has been challenged by the use of several sequential unit operations and the frequent use of hazardous and flammable solvents to produce defatted flours for subsequent protein extraction. The effects of aqueous (AEP) and enzymatic extraction (EAEP) on the simultaneous extraction of lipids and proteins from full-fat almond flour, insoluble microstructure, oil recovery from the oil-rich emulsion, and physicochemical and functional properties of the extracted protein were evaluated. Except for the use of 0.5% of protease in the EAEP, extraction parameters were similar for both processes (pH 9.0, 50 ºC, 1:10 solids-to-liquid ratio, and 60 min). Enzymatic extraction significantly improved the oil (from 62 to 67%) and protein (from 67 to 77%) extractability while generating smaller protein fragments and creating a more porous insoluble structure. EAEP followed by enzymatic destabilization of the oil-rich emulsion increased the degree of hydrolysis of the emulsion proteins from 8 to 22% while reducing its hydrophobicity from 1205 to 688, resulting in 93% oil recovery. EAEP also resulted in the production of protein extracts with higher protein content, a more unordered protein secondary structure with reduced surface hydrophobicity, and reduced thermostability. Importantly, proteolysis significantly enhanced the functionality of the hydrolysates at pH values close to the almond protein isoelectric point. At pH 5.0, the hydrolysates had higher solubility (47 vs 23%), emulsification capacity (492 vs 402 g oil/ g protein), emulsification activity index (35 vs 17 m2 40 /g), and foaming capacity (23 vs 41 11%) compared with unhydrolyzed proteins. These results highlight the effectiveness of this flammable solvent-free extraction approach to maximize lipid and protein extractability from almond flour with concurrent improvement in oil recovery and protein functionality, creating new opportunities for their application as food ingredients.
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Arora, Bhumika. "Refinement of G protein-coupled receptor structure models." In BCB '20: 11th ACM International Conference on Bioinformatics, Computational Biology and Health Informatics. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3388440.3414920.

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Reports on the topic "G-protein"

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Neale, Christopher Andrew, and Angel Enrique Garcia. Regulation of Intercellular Signaling by G protein-coupled receptors. Office of Scientific and Technical Information (OSTI), February 2019. http://dx.doi.org/10.2172/1496726.

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Boston, Mark E., G. C. Frech, Enrique Chacon-Cruz, E. S. Buescher, and David G. Oelberg. Surfactant Releases Internal Calcium Stores in Neutrophils by G Protein-Mediated Pathway. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada413640.

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Liu, Mingyao. Role of a Novel Prostate-Specific G-Protein Coupled Receptor (PSGR) in Prostate Tumor Development. Fort Belvoir, VA: Defense Technical Information Center, February 2003. http://dx.doi.org/10.21236/ada415521.

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Rafaeli, Ada, and Russell Jurenka. Molecular Characterization of PBAN G-protein Coupled Receptors in Moth Pest Species: Design of Antagonists. United States Department of Agriculture, December 2012. http://dx.doi.org/10.32747/2012.7593390.bard.

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The proposed research was directed at determining the activation/binding domains and gene regulation of the PBAN-R’s thereby providing information for the design and screening of potential PBAN-R-blockers and to indicate possible ways of preventing the process from proceeding to its completion. Our specific aims included: (1) The identification of the PBAN-R binding domain by a combination of: (a) in silico modeling studies for identifying specific amino-acid side chains that are likely to be involved in binding PBAN with the receptor and; (b) bioassays to verify the modeling studies using mutant receptors, cell lines and pheromone glands (at tissue and organism levels) against selected, designed compounds to confirm if compounds are agonists or antagonists. (2) The elucidation ofthemolecular regulationmechanisms of PBAN-R by:(a) age-dependence of gene expression; (b) the effect of hormones and; (c) PBAN-R characterization in male hair-pencil complexes. Background to the topic Insects have several closely related G protein-coupled receptors (GPCRs) belonging to the pyrokinin/PBAN family, one with the ligand pheromone biosynthesis activating neuropeptide or pyrokinin-2 and another with diapause hormone or pyrokinin-1 as a ligand. We were unable to identify the diapause hormone receptor from Helicoverpa zea despite considerable effort. A third, related receptor is activated by a product of the capa gene, periviscerokinins. The pyrokinin/PBAN family of GPCRs and their ligands has been identified in various insects, such as Drosophila, several moth species, mosquitoes, Triboliumcastaneum, Apis mellifera, Nasoniavitripennis, and Acyrthosiphon pisum. Physiological functions of pyrokinin peptides include muscle contraction, whereas PBAN regulates pheromone production in moths plus other functions indicating the pleiotropic nature of these ligands. Based on the alignment of annotated genomic sequences, the primary and secondary structures of the pyrokinin/PBAN family of receptors have similarity with the corresponding structures of the capa or periviscerokinin receptors of insects and the neuromedin U receptors found in vertebrates. Major conclusions, solutions, achievements Evolutionary trace analysisof receptor extracellular domains exhibited several class-specific amino acid residues, which could indicate putative domains for activation of these receptors by ligand recognition and binding. Through site-directed point mutations, the 3rd extracellular domain of PBAN-R was shown to be critical for ligand selection. We identified three receptors that belong to the PBAN family of GPCRs and a partial sequence for the periviscerokinin receptor from the European corn borer, Ostrinianubilalis. Functional expression studies confirmed that only the C-variant of the PBAN-R is active. We identified a non-peptide agonist that will activate the PBAN-receptor from H. zea. We determined that there is transcriptional control of the PBAN-R in two moth species during the development of the pupa to adult, and we demonstrated that this transcriptional regulation is independent of juvenile hormone biosynthesis. This transcriptional control also occurs in male hair-pencil gland complexes of both moth species indicating a regulatory role for PBAN in males. Ultimate confirmation for PBAN's function in the male tissue was revealed through knockdown of the PBAN-R using RNAi-mediated gene-silencing. Implications, both scientific and agricultural The identification of a non-peptide agonist can be exploited in the future for the design of additional compounds that will activate the receptor and to elucidate the binding properties of this receptor. The increase in expression levels of the PBAN-R transcript was delineated to occur at a critical period of 5 hours post-eclosion and its regulation can now be studied. The mysterious role of PBAN in the males was elucidated by using a combination of physiological, biochemical and molecular genetics techniques.
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Barefoot, Susan F., Bonita A. Glatz, Nathan Gollop, and Thomas A. Hughes. Bacteriocin Markers for Propionibacteria Gene Transfer Systems. United States Department of Agriculture, June 2000. http://dx.doi.org/10.32747/2000.7573993.bard.

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The antibotulinal baceriocins, propionicin PLG-1 and jenseniin G., were the first to be identified, purified and characterized for the dairy propionibaceria and are produced by Propionibacterium thoenii P127 and P. thoenii/jensenii P126, respectively. Objectives of this project were to (a) produce polyclonal antibodies for detection, comparison and monitoring of propionicin PLG-1; (b) identify, clone and characterize the propionicin PLG-1 (plg-1) and jenseniin G (jnG) genes; and (3) develop gene transfer systems for dairy propionibacteria using them as models. Polyclonal antibodies for detection, comparison and monitoring of propionicin PLG-1 were produced in rabbits. Anti-PLG-1 antiserum had high titers (256,000 to 512,000), neutralized PLG-1 activity, and detected purified PLG-1 at 0.10 mg/ml (indirect ELISA) and 0.033 mg/ml (competitive indirect ELISA). Thirty-nine of 158 strains (most P. thoenii or P. jensenii) yielded cross-reacting material; four strains of P. thoenii, including two previously unidentified bacteriocin producers, showed biological activity. Eight propionicin-negative P127 mutants produced neither ELISA response nor biological activity. Western blot analyses of supernates detected a PLG-1 band at 9.1 kDa and two additional protein bands with apparent molecular weights of 16.2 and 27.5 kDa. PLG-1 polyclonal antibodies were used for detection of jenseniin G. PLG-1 antibodies neutralized jenseniin G activity and detected a jenseniin G-sized, 3.5 kDa peptide. Preliminary immunoprecipitation of crude preparations with PLG-1 antibodies yielded three proteins including an active 3-4 kDa band. Propionicin PLG-1 antibodies were used to screen a P. jensenii/thoenii P126 genomic expression library. Complete sequencing of a cloned insert identified by PLG-1 antibodies revealed a putative response regulator, transport protein, transmembrane protein and an open reading frame (ORF) potentially encoding jenseniin G. PCR cloning of the putative plg-1 gene yielded a 1,100 bp fragment with a 355 bp ORF encoding 118 amino acids; the deduced N-terminus was similar to the known PLG-1 N-terminus. The 118 amino acid sequence deduced from the putative plg-1 gene was larger than PLG-1 possibly due to post-translational processing. The product of the putative plg-1 gene had a calculated molecular weight of 12.8 kDa, a pI of 11.7, 14 negatively charged residues (Asp+Glu) and 24 positively charged residues (Arg+Lys). The putative plg-1 gene was expressed as an inducible fusion protein with a six-histidine residue tag. Metal affinity chromatography of the fused protein yielded a homogeneous product. The fused purified protein sequence matched the deduced putative plg-1 gene sequence. The data preliminarily suggest that both the plg-1 and jnG genes have been identified and cloned. Demonstrating that antibodies can be produced for propionicin PLG-1 and that those antibodies can be used to detect, monitor and compare activity throughout growth and purification was an important step towards monitoring PLG-1 concentrations in food systems. The unexpected but fortunate cross-reactivity of PLG-1 antibodies with jenseniin G led to selective recovery of jenseniin G by immunoprecipitation. Further refinement of this separation technique could lead to powerful affinity methods for rapid, specific separation of the two bacteriocins and thus facilitate their availability for industrial or pharmaceutical uses. Preliminary identification of genes encoding the two dairy propionibacteria bacteriocins must be confirmed; further analysis will provide means for understanding how they work, for increasing their production and for manipulating the peptides to increase their target species. Further development of these systems would contribute to basic knowledge about dairy propionibacteria and has potential for improving other industrially significant characteristics.
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Chen, Songhai, and Yuanchao Ye. Targeting G-Protein Signaling for the Therapeutics of Prostate Tumor Bone Metastases and the Associated Chronic Bone Pain. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada609444.

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Chen, Songhai, and Prakash Paudyal. Targeting G-Protein Signaling for the Therapeutics of Prostate Tumor Bone Metastases and the Associated Chronic Bone Pain. Fort Belvoir, VA: Defense Technical Information Center, September 2015. http://dx.doi.org/10.21236/ada632402.

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Chen, Songhai, and Yuanchao Ye. Targeting G-Protein Signaling for the Therapeutics of Prostate Tumor Bone Metastases and the Associated Chronic Bone Pain. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada584250.

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Heitman, Joseph. Novel Gbeta Mimic Kelch Proteins (Gpb1 and Gpb2 Connect G-Protein Signaling to Ras via Yeast Neurofibromin Homologs Ira1 and Ira2: A Model for Human NF1. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada483900.

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Heitman, Joseph, and Toshiaki Harashima. Novel Gbeta Mimic Kelch Proteins (Gpb1 and Gpb2 Connect G-Protein Signaling to Ras via Yeast Neurofibromin Homologs Ira1 and Ira2. A Model for Human NF1. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada479028.

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