Relevant bibliographies by topics / G proteins

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'G proteins'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "G proteins"

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Anderson, Alexandra, and Rachel McMullan. "G-proteins." Worm 1, no. 4 (October 2012): 196–201. http://dx.doi.org/10.4161/worm.20466.

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Yost, C. Spencer. "G Proteins." Anesthesia & Analgesia 77, no. 4 (October 1993): 822???834. http://dx.doi.org/10.1213/00000539-199310000-00029.

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Mollenhauer, Juergen. "G PROTEINS." Shock 6, no. 3 (September 1996): 230. http://dx.doi.org/10.1097/00024382-199609000-00013.

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Roche, Patrick C. "G PROTEINS." Shock 6 (September 1996): 230. http://dx.doi.org/10.1097/00024382-199609010-00013.

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Under, Maurine E., and Alfred G. Gilman. "G Proteins." Scientific American 267, no. 1 (July 1992): 56–65. http://dx.doi.org/10.1038/scientificamerican0792-56.

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RAWLS, REBECCA L. "G-Proteins." Chemical & Engineering News 65, no. 51 (December 21, 1987): 26–39. http://dx.doi.org/10.1021/cen-v065n051.p026.

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Milligan, G. "G-proteins." FEBS Letters 279, no. 1 (February 11, 1991): 157–58. http://dx.doi.org/10.1016/0014-5793(91)80274-7.

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Dolphin, Annette. "G proteins." Trends in Neurosciences 14, no. 4 (April 1991): 160–61. http://dx.doi.org/10.1016/0166-2236(91)90093-a.

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Giershik, Peter. "G proteins." Trends in Biochemical Sciences 15, no. 11 (November 1990): 448. http://dx.doi.org/10.1016/0968-0004(90)90289-n.

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Hepler, John R., and Alfred G. Gilman. "G proteins." Trends in Biochemical Sciences 17, no. 10 (October 1992): 383–87. http://dx.doi.org/10.1016/0968-0004(92)90005-t.

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Dissertations / Theses on the topic "G proteins"

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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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Nauli, Sehat. "Folding kinetics and redesign of Peptostreptococcal protein L and G /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/9237.

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Nguyen, Giang Huong. "A functional analysis of the human LPA₁G protein coupled receptor." Thesis, Available online, Georgia Institute of Technology, 2004:, 2004. http://etd.gatech.edu/theses/available/etd-06072004-131304/unrestricted/nguyen%5Fgiang%5Fh%5F200405%5Fms.pdf.

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Ghimire, 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.

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Drinnan, Suzane Loraine. "G proteins in the basal ganglia." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/28981.

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G proteins are alpha-beta-gamma heterotrimers in the resting state, bound to GDP and complexed with the unbound receptor. Once the receptor becomes occupied, the alpha subunit exchanges GDP for GTP, becomes activated, and dissociates from the receptor and can stimulate or inhibit many intracellular activities such as phosphorylation and channel conductance. For example, Gs and Golf alpha subunits stimulate and Gi alpha subunits inhibit adenylyl cyclase. Go alpha subunits are abundant in brain, but are of unknown function. cDNAs for the alpha subunit have been cloned. In order to examine the relative distributions of G proteins in the brain, we used in situ hybridization with radiolabelled synthetic oligonucleotide probes. By using a tyrosine hydroxylase antibody, we found that the dopaminergic neurons of the substantia nigra and the noradrenergic neurons of the locus ceruleus express mRNA for the alpha subunits for each of Gi, Go, and Gs. We noted a paucity of Gs mRNA in the striatum. This was surprising because the basal ganglia contain a dopamine-stimulated adenylyl cyclase activity which has been assumed to be transduced by Gs. Also, immunohistochemistry, immunoblotting, and cholera ADP-ribosylation indicated a very high level of Gs alpha-like protein in the striatum. In order to ascertain which specific G protein we were detecting, we made probes to a new G protein previously identified in the olfactory system. Golf is a stimulatory G protein with size and sequence characteristics similar to those of Gs. The cholera toxin ADP-ribosylation site and C-terminal region to which the antibody was made are identical. We made oligonucloetide probes to the translated and untranslated portions of Golf alpha. High levels Golf mRNA and protein were detected in the striatum and nucleus accumbens, in addition to the expected high levels in the olfactory tubercle. Northern blot studies indicated that Golf transcripts are approximately ten-fold more abundant than Gs alpha transcripts in the striatum. These data indicate that Golf in not an olfactory-specific G protein. It is also the major stimulatory G protein in the basal ganglia. The selective expression of high levels of Golf in dopamine-rich forebrain areas suggest that it may couple DI dopamine receptors to adenylyl cyclase. The role of Golf in dopaminergic neurotransmission and neuropsychiatric disease should be considered.
Medicine, Faculty of
Graduate
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Hodson, Elizabeth Anne Marie. "G protein regulation of phospholipase C in vascular smooth muscle." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390487.

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Song, Hongman. "The roles of the phosducin family proteins in the regulation of heterotrimeric G proteins in vertebrate photoreceptors." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10413.

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Thesis (Ph. D.)--West Virginia University, 2009.
Title from document title page. Document formatted into pages; contains vi, 96 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Brownlie, Zoe. "Regulation of signal transduction by RGS4." Connect to e-thesis, 2007. http://theses.gla.ac.uk/124/.

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Thesis (Ph.D.) - University of Glasgow, 2007.
Ph.D. thesis submitted to the Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, 2007. Includes bibliographical references.
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Adhikari, Anirban. "Regulation of guanine nucelotide exchange in inhibitory G protein alpha subunit by activator of G protein signaling 3 and novel regulatory peptides." Embargoed access until after 12/19/2006, 2005. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=114.

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Han, 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.

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Books on the topic "G proteins"

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Ravi, Iyengar, and Birnbaumer Lutz, eds. G proteins. San Diego: Academic Press, 1990.

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Graeme, Milligan, Wakelam M. J. O, and Kay J, eds. G-proteins and signal transduction. London: Biochemical Society, 1990.

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Graeme, Milligan, Wakelam Michael, Kay J, and Biochemical Society, eds. G-proteins and signal transduction. London: Biochemical Society, 1990.

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M, Spiegel Allen, ed. G proteins. Austin, TX: R.G. Landes Co., 1994.

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Pennington, Stephen R. GTP-binding proteins 1: heterotrimeric G proteins. London: Academic Press, 1994.

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Pennington, Stephen R. GTP-binding proteins 1: heterotrimeric G proteins. London: Academic Press, 1995.

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Hébert, Terence E., and Bruce G. Allen. Nuclear G-protein coupled receptors: Methods and protocols. New York: Humana Press, 2015.

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Jeanteur, Philippe, ed. Cytoskeleton and Small G Proteins. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58591-3.

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Spiegel, Allen M., ed. G Proteins, Receptors, and Disease. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1802-9.

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R, Manning David, ed. G proteins: Techniques of analysis. Boca Raton: CRC Press, 1999.

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Book chapters on the topic "G proteins"

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Worzfeld, Thomas, and Stefan Offermanns. "G Proteins." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_2295-5.

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Neer, Eva J. "G Proteins." In Protein Design and the Development of New Therapeutics and Vaccines, 143–53. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5739-1_7.

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Worzfeld, Thomas, and Stefan Offermanns. "G Proteins." In Encyclopedia of Cancer, 1819–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_2295.

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Worzfeld, Thomas, and Stefan Offermanns. "G-Proteins." In Encyclopedia of Cancer, 1587–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2295.

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Gooch, Jan W. "G Proteins." In Encyclopedic Dictionary of Polymers, 896. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13854.

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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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Belyi, Yuri F. "Heterotrimeric G Proteins." In Intracellular Parasitism of Microorganisms, 31–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22047-4_2.

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Chiosi, E., A. Spina, F. Valente, and G. Illiano. "Protein Kinase C and G Proteins." In Adenine Nucleotides in Cellular Energy Transfer and Signal Transduction, 257–68. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7315-4_23.

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Conference papers on the topic "G proteins"

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Xiao, Xuliang, and Yiding Zhao. "G-proteins and G-protein receptors in diseases." In Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), edited by Alan Wang. SPIE, 2024. http://dx.doi.org/10.1117/12.3021708.

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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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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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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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Lapetina, Eduardo G. "THE ROLE OF INOSITIDES, PHOSPHOLIPASE C AND G-PROTEINS IN RECEPTOR TRANSDUCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644775.

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It is now widely recognized that the activation of phospholipase C by specific agonists leads to the formation of two second messengers: (1) inositol trisphosphate, which releases Ca2+ from the endoplasmic reticulum to the cytosol and (2) 1,2- diacylglycerol, which stimulates protein kinase C. In the past few years, GTP-binding proteins have been associated with the regulation of phospholipase C. However, the identity of the GTP-binding protein involved and the type of association with phospholipase C is not yet known. It is now recognized that there are two types of phospholipase C enzymes: (a) a soluble enzyme that has been characterized in several tissues and does not preferentially hydrolyze polyphospholinositides and (b) membrane-bound enzymes that are coupled to the receptors, specifically hydrolyzing polyphosphoinositides and activated by membrane guanine nucleotide-binding proteins. Recent reports have tried to assess the involvement of GTP-binding proteins in the agonist-induced stimulation of phospholipase C, and various related aspects have been reported. These are concerned with: (a) detection of various GTP-binding proteins in platelets, (b) the effects of known inhibitors of GTP-binding proteins such as GDPgS or pertussis toxin on the agonist-induced stimulation of phospholipase C, (c) the direct effects of stimulators of GTP-binding proteins such as GTP, GTP-analogs and fluoride on phospholipase C activity, (d) the possible association of GTP-binding proteins to cytosolic phospholipase C that would then lead to degradation of the membrane-bound inositides and (e) cytosolic phospholipase C response to the activation of cell surface receptors. The emerging information has had contradictory conclusions. (1) Pretreatment of saponin-permeabilized platelets with pertussis toxin has been shown to enhance and to inhibit the thrombin-induced activation of phospholipase C. Therefore, it is not clear if a G protein that is affected by pertussis toxin in a manner similar to Gi or Go plays a central role in activation of phospholipase C. (2) Studies on the effect of GDPβ;S are also conflicting indicating that there may be GTP-independent and/or -dependent pathways for the activation of phosphoinositide hydrolysis. (3) A cytosolic phospholipase C is activated by GTP, and it has been advanced that this activity might trigger the hydrolysis of membrane-bound inositides. A cytosolic GTP-binding protein might be involved in this action, and it is speculated that an α-subunit might be released to the cytoplasm by a receptor-coupled mechanism to activate phospholipase C. However, no direct evidence exists to support this conclusion. Moreover, the exact contribution of phospholipase C from the membranes or the cytosol to inositide hydrolysis in response to cellular agonists and the relationship of those activites to membrane-bound or soluble GTP-binding proteins are unknown. Our results indicate that the stimulation of phospholipase C in platelets by GDPβS and thrombin are affected differently by GDPβS. GDPgSinhibits the formation of inositol phosphates produced by GTPγS but not that induced by thrombin. Thrombin, therefore, can directly stimulate phospholipase C without the involvement of a “stimulatory” GTP-binding protein, such as Gs, for the agonist stimulation of adenylate cyclase. However, an “inhibitory” GTP-binding protein might have some influence on thrombin-stimulated phospholipase C, since in the presence of GDPγS thrombin produces a more profound stimulation of phospholipase C.This “inhibitory” GTP-binding protein might be ADP-ribosylated by pertussis toxin because pertussis toxin can also enhance thrombin action on phospholipase C activity. Therefore, phospholipase C that responds to thrombin could be different from the one that responds to GTPγS. Cytosolic phospholipase C can be activated by GTP or GTP analogs, and the one that responds to thrombin should be coupled to the receptors present in the plasma membrane. The initial action of thrombin is to directly activate the plasma membrane-bound phospholipase C and the mechanism of this activation is probably related to the proteolytic action of thrombin or the activation of platelet proteases by thrombin. In agreement with this, trypsin can also directly activate platelet phospholipase C and, subsequently, GTPyS produces further activation of phospholipase C. If these two mechanisms are operative in platelets, the inhibition of cytosolic phospholipase C by GDPβS would allow a larger fraction of inositides for degradation of the thrombin-stimulated phospholipase C, as our results show.
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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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Jeganathan, Brasathe, Feral Temelli, and Thavaratnam Vasanthan. "Functional properties of faba bean proteins extracted by different aqueous processes for food applications." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/phkb7574.

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Dry fractionation of faba bean protein is a sustainable alternative to energy-intensive wet fractionation approaches. However, it can only lead to relatively modest enrichment in protein content. The primary goal of this study was to compare the impact of aqueous protein extraction processes on the functionalities of faba bean proteins for food applications. Proteins from two Canadian faba bean cultivars Snowbird (zero-tannin, ZT) and Athena (high-tannin, HT) were extracted by dialysis following water extraction (W) and salt extraction (S) processes, and conventional alkali-acid approach (A). Although salt-soluble globulins were the primary proteins found in faba beans based on Osborne's protein classification, protein isolates (PIs) from ZT-W and HT-W had significantly higher (P< 0.05) protein contents on a dry matter basis (89.8±0.4% and 92.0±0.0%, respectively, Nx6.25) as compared to protein concentrates (PCs) from ZT-S (78.2±0.4%) and HT-S (77.7±0.2%). These differences in protein extractability could be attributed to the higher levels of naturally present minerals. Substantially lower (P< 0.05) mineral contents were detected in HT in comparison to ZT, plausibly due to the affinity of tannins towards minerals. Calorimetric analysis of W-PIs and A-PIs maintained at low-moisture contents resulted in a very high denaturation temperature range (225-235°C), implying their thermal stability for high-temperature processing. Furthermore, solubility, foaming and emulsification properties, and hydration capacities of W-PIs were higher or comparable to those of A-PIs and S-PCs. Dynamic rheological studies (25€“95€“25 °C) of W-PI heat-induced gels indicated that storage modulus (G') and loss modulus (G'') increased over time with an early crossover point (G' > G'') as compared to A-PIs. The stress and strain at fracture of W-PIs and A-PIs gels were comparable to those of whole egg gels. In summary, W-PIs were superior to S-PCs in terms of their functionalities and can be considered chemical-free alternatives to A-PIs, for sustainable food applications.
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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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Branković, Jovica, Zorica D. Petrović, and Vladimir P. Petrović. "Phenolic N-acyl hydrazone derivatives: In silico assessment of potential antibacterial activity against selected G+ and G- strains." In 2nd International Conference on Chemo and Bioinformatics. Institute for Information Technologies, University of Kragujevac, 2023. http://dx.doi.org/10.46793/iccbi23.491b.

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In this work, a series of phenolic N-acyl hydrazones was investigated in silico against six selected E. coli and S. aureus bacterial proteins. Generally, the obtained molecular docking results revealed significantly higher binding affinities of analogs a–n towards selected enzymes in comparison to standard compounds. In the case of E. coli proteins 1hnj, 1c14, and 6ntw, the lowest binding energies were calculated for derivatives l (-8.5 kcal/mol), d (-9.0 kcal/mol), and k (-8.2 kcal/mol), respectively. On the other hand, the highest binding affinity towards the S. aureus 3u2d, 1mwu, and 1jij enzymes was expressed by derivatives a, d, and j, with binding energies of -8.3, -8.4, and -9.4 kcal/mol, respectively. The obtained in silico results indicate the potential inhibitory activity of selected phenolic N-acyl hydrazone derivatives against E. coli and S. aureus bacterial proteins and represent a valuable ground base for future in vitro experiments.
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Zhang Fan, Liu Zhicheng, Li Xia, Gao Zhiwen, and Su Xuan. "Functional Site Analysis in Proteins of G Protein Signaling Pathways Using Fuzzy Evolutionary Trace Method." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1615537.

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Reports on the topic "G proteins"

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Banai, Menachem, and Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7568100.bard.

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The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
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Ohad, Nir, and Robert Fischer. Regulation of Fertilization-Independent Endosperm Development by Polycomb Proteins. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695869.bard.

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Arabidopsis mutants that we have isolated, encode for fertilization-independent endosperm (fie), fertilization-independent seed2 (fis2) and medea (mea) genes, act in the female gametophyte and allow endosperm to develop without fertilization when mutated. We cloned the FIE and MEA genes and showed that they encode WD and SET domain polycomb (Pc G) proteins, respectively. Homologous proteins of FIE and MEA in other organisms are known to regulate gene transcription by modulating chromatin structure. Based on our results, we proposed a model whereby both FIE and MEA interact to suppress transcription of regulatory genes. These genes are transcribed only at proper developmental stages, as in the central cell of the female gametophyte after fertilization, thus activating endosperm development. To test our model, the following questions were addressed: What is the Composition and Function of the Polycomb Complex? Molecular, biochemical, genetic and genomic approaches were offered to identify members of the complex, analyze their interactions, and understand their function. What is the Temporal and Spatial Pattern of Polycomb Proteins Accumulation? The use of transgenic plants expressing tagged FIE and MEA polypeptides as well as specific antibodies were proposed to localize the endogenous polycomb complex. How is Polycomb Protein Activity Controlled? To understand the molecular mechanism controlling the accumulation of FIE protein, transgenic plants as well as molecular approaches were proposed to determine whether FIE is regulated at the translational or posttranslational levels. The objectives of our research program have been accomplished and the results obtained exceeded our expectation. Our results reveal that fie and mea mutations cause parent-of-origin effects on seed development by distinct mechanisms (Publication 1). Moreover our data show that FIE has additional functions besides controlling the development of the female gametophyte. Using transgenic lines in which FIE was not expressed or the protein level was reduced during different developmental stages enabled us for the first time to explore FIE function during sporophyte development (Publication 2 and 3). Our results are consistent with the hypothesis that FIE, a single copy gene in the Arabidopsis genome, represses multiple developmental pathways (i.e., endosperm, embryogenesis, shot formation and flowering). Furthermore, we identified FIE target genes, including key transcription factors known to promote flowering (AG and LFY) as well as shoot and leaf formation (KNAT1) (Publication 2 and 3), thus demonstrating that in plants, as in mammals and insects, PcG proteins control expression of homeobox genes. Using the Yeast two hybrid system and pull-down assays we demonstrated that FIE protein interact with MEA via the N-terminal region (Publication 1). Moreover, CURLY LEAF protein, an additional member of the SET domain family interacts with FIE as well. The overlapping expression patterns of FIE, with ether MEA or CLF and their common mutant phenotypes, demonstrate the versatility of FIE function. FIE association with different SET domain polycomb proteins, results in differential regulation of gene expression throughout the plant life cycle (Publication 3). In vitro interaction assays we have recently performed demonstrated that FIE interacts with the cell cycle regulatory component Retinobalsoma protein (pRb) (Publication 4). These results illuminate the potential mechanism by which FIE may restrain embryo sac central cell division, at least partly, through interaction with, and suppression of pRb-regulated genes. The results of this program generated new information about the initiation of reproductive development and expanded our understanding of how PcG proteins regulate developmental programs along the plant life cycle. The tools and information obtained in this program will lead to novel strategies which will allow to mange crop plants and to increase crop production.
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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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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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Heitman, Joseph, and Toshiaki Harashima. Novel Gbeta Mimic Kelch Proteins Gpb1 and Gpb2 Connect G-Protein Signaling to Ras Via Yeast Neurofibromin Homologs Ira 1 and Ira 2: A Model for Human NF1. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada446943.

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Heitman, Joseph. Novel Gbeta Mimic Kelch Proteins Gpb1 and Gpb2 Connect G-Protein Signaling to Ras via Yeast Neurofibromin Homologs Ira 1 and Ira 2: A Model for Human NF1. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada469875.

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8

Grafi, Gideon, and Brian Larkins. Endoreduplication in Maize Endosperm: An Approach for Increasing Crop Productivity. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575285.bard.

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The focus of this research project is to investigate the role of endoreduplication in maize endosperm development and the extent to which this process contributes to high levels of starch and storage protein synthesis. Although endoreduplication has been widely observed in many cells and tissues, especially those with high levels of metabolic activity, the molecular mechanisms through which the cell cycle is altered to produce consecutive cycles of S-phase without an intervening M-phase are unknown. Our previous research has shown that changes in the expression of several cell cycle regulatory genes coincide with the onset of endoreduplication. During this process, there is a sharp reduction in the activity of the mitotic cyclin-dependent kinase (CDK) and activation of the S-phase CDK. It appears the M-phase CDK is stable, but its activity is blocked by a proteinaceous inhibitor. Coincidentally, the S-phase checkpoint protein, retinoblastoma (ZmRb), becomes phosphorylated, presumably releasing an E2F-type transcriptional regulator which promotes the expression of genes responsible for DNA synthesis. To investigate the role of these cell cycle proteins in endoreduplication, we have created transgenic maize plants that express various genes in an endosperm-specific manner using a storage protein (g-zein) promoter. During the first year of the grant, we constructed point mutations of the maize M-phase kinase, p34cdc2. One alteration replaced aspartic acid at position 146 with asparagine (p3630-CdcD146N), while another changed threonine 161 to alanine (p3630-CdcT161A). These mutations abolish the activity of the CDK. We hypothesized that expression of the mutant forms of p34cdc2 in endoreduplicating endosperm, compared to a control p34cdc2, would lead to extra cycles of DNA synthesis. We also fused the gene encoding the regulatory subunit of the M- phase kinase, cyclin B, under the g-zein promoter. Normally, cyclin B is expected to be destroyed prior to the onset of endoreduplication. By producing high levels of this protein in developing endosperm, we hypothesized that the M-phase would be extended, potentially reducing the number of cycles of endoreduplication. Finally, we genetically engineered the wheat dwarf virus RepA protein for endosperm-specific expression. RepA binds to the maize retinoblastoma protein and presumably releases E2F-like transcription factors that activate DNA synthesis. We anticipated that inactivation of ZmRb by RepA would lead to additional cycles of DNA synthesis.
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Splitter, Gary, Zeev Trainin, and Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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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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