Relevant bibliographies by topics / Protein mechanism

Academic literature on the topic 'Protein mechanism'

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Published: 14 March 2023

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Journal articles on the topic "Protein mechanism"

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Schreiber, G., D. Reichmann, M. Cohen, Y. Pillip, O. Rahat, O. Dym, V. Potapov, V. Sobolev, and M. Edelman. "Protein–protein interaction: from mechanism to protein design." Acta Crystallographica Section A Foundations of Crystallography 63, a1 (August 22, 2007): s18. http://dx.doi.org/10.1107/s0108767307099606.

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Gianni, Stefano, Nicoletta Calosci, Jan M. A. Aelen, Geerten W. Vuister, Maurizio Brunori, and Carlo Travaglini-Allocatelli. "Kinetic folding mechanism of PDZ2 from PTP-BL." Protein Engineering, Design and Selection 18, no. 8 (July 25, 2005): 389–95. http://dx.doi.org/10.1093/protein/gzi047.

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Barford, D. "The mechanism of protein kinase regulation by protein phosphatases." Biochemical Society Transactions 29, no. 4 (August 1, 2001): 385–91. http://dx.doi.org/10.1042/bst0290385.

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Protein kinases are an important class of substrate of the protein phosphatases. We have examined the mechanism of dephosphorylation of the activation segments of the insulin receptor kinase and cyclin-dependent kinase 2 by their respective phosphatases, namely the tyrosine specific phosphatase PTP1B and the dual specificity phosphatase KAP. These studies reveal that PTP1B and KAP utilize contrasting mechanisms in order to dephosphorylate their substrates specifically.
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HIROSE, Masaaki. "Folding Mechanism of Protein." Kagaku To Seibutsu 36, no. 5 (1998): 290–96. http://dx.doi.org/10.1271/kagakutoseibutsu1962.36.290.

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Wong, Chi-Ming, Lucia Marcocci, Dividutta Das, Xinhong Wang, Haibei Luo, Makhosazane Zungu-Edmondson, and Yuichiro J. Suzuki. "Mechanism of protein decarbonylation." Free Radical Biology and Medicine 65 (December 2013): 1126–33. http://dx.doi.org/10.1016/j.freeradbiomed.2013.09.005.

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Yoshimura, Takatoshi, Hidehiko Noguchi, Takayuki Inoue, and Nobuhiko Saitô. "Mechanism of protein folding." Biophysical Chemistry 40, no. 3 (July 1991): 277–91. http://dx.doi.org/10.1016/0301-4622(91)80026-n.

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Watanabe, Kazunori, Atsuhiko Nakamura, Yoshinori Fukuda, and Nobuhiko Saitô. "Mechanism of protein folding." Biophysical Chemistry 40, no. 3 (July 1991): 293–301. http://dx.doi.org/10.1016/0301-4622(91)80027-o.

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N�lting, Bengt, and Karl Andert. "Mechanism of protein folding." Proteins: Structure, Function, and Genetics 41, no. 3 (2000): 288–98. http://dx.doi.org/10.1002/1097-0134(20001115)41:3<288::aid-prot20>3.0.co;2-c.

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Zheng, Ya-Jun, Kenneth M. Merz, and Gregory K. Farber. "Theoretical examination of the mechanism of aldose–ketose isomerization." "Protein Engineering, Design and Selection" 6, no. 5 (1993): 479–84. http://dx.doi.org/10.1093/protein/6.5.479.

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Abaturov, A. E., and V. L. Babуch. "Mechanisms of action of cytoplasmic microRNAs. Part 3. TNRC6-associated mechanism of miRNA-mediated mRNA degradation." CHILD`S HEALTH 17, no. 4 (September 20, 2022): 209–16. http://dx.doi.org/10.22141/2224-0551.17.4.2022.1519.

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The scientific review presents the mechanisms of action of cytoplasmic miRNAs, namely posttranscriptional silencing: the TNRC6-associated mechanism of miRNA-mediated mRNA degradation. To write the article, information was searched using databases Scopus, Web of Science, MedLine, PubMed, Google Scholar, EMBASE, Global Health, The Cochrane Library, CyberLeninka. It is known that in the cytoplasm of cells in cases of short region, miRNA complementarities cause posttranscriptional silencing, using the first of the main molecular mechanisms: the TNRC6-associated mechanism of miRNA-mediated mRNA degradation. Mammalian AGO proteins have been shown to contain the conserved m7G-cap-binding protein motif (known as the MID domain), which is required to induce microRNA-mediated translation repression. After binding of this AGO motif to ­microRNAs, TNRC6 proteins (GW182) are recruited that, in turn, recruits various proteins (PABPC1, PAN3 and NOT1) involved in the induction of the target gene silencing. The authors state that tryptophan residues, which are placed in the hydrophobic pockets of TNRC6 protein partners, cause a high degree of affinity and specificity of interactions. Scientists believe that the TNRC6 protein when interacting with AGO proteins can simultaneously use three GW/WG repeats (motif 1, motif 2 and hook motif), which are located in the Argonaute-binding domain. Therefore, the TNRC6 protein can bind to three AGO molecules simultaneously. TNRC6 proteins are known to be PABP-interac­ting proteins whose interaction with PABP is mediated by conservative PABP-binding motif 2. TNRC6 proteins have been shown to interact with the cytoplasmic PABPC1 protein during mRNA translation and stabilization. It is shown that the CCR4-NOT protein complex is a highly conserved multifunctional multiprotein formation having 3’-5’-exoribonuclease activity, due to which it controls mRNA metabolism. Thus, the TNRC6-associated me­chanism of miRNA-mediated mRNA degradation in the cytoplasm of the cell causes posttranscriptional silencing. In this mechanism, there is an interaction of TNRC6 with PABPC1 protein, recruitment of deadenylating complexes PAN2-PAN3 and CCR4-NOT by the TNRC6 proteins.
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Dissertations / Theses on the topic "Protein mechanism"

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Fang, Lin. "Mechanism of client protein binding by heat shock protein 90 /." view abstract or download file of text, 2006. http://proquest.umi.com/pqdweb?did=1251819301&sid=2&Fmt=2&clientId=11238&RQT=309&VName=PQD.

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Thesis (Ph. D.)--University of Oregon, 2006.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 115-121). Also available for download via the World Wide Web; free to University of Oregon users.
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Smart, Nicola. "Studies on the mechanism of protein kinase C down-regulation." Thesis, Royal Veterinary College (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391675.

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Lai, Chun Wan Jeffrey. "Mechanism of G Protein Beta-Gamma Assembly Mediated by Phosducin-Like Protein 1." BYU ScholarsArchive, 2011. https://scholarsarchive.byu.edu/etd/3190.

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G-protein coupled receptor signaling (GPCR) is essential for regulating a large variety of hormonal, sensory and neuronal processes in eukaryotic cells. Because the regulation of these physiological responses is critical, GPCR signaling pathways are carefully controlled at different levels within the cascade. Phosducin-like protein 1 (PhLP1) can bind the G protein βγ dimer and participate in GPCR signaling. Recent evidence has supported the concept that PhLP1 can serve as a co-chaperone of the eukaryotic cytosolic chaperonin complex CCT/TRiC to mediate G βγ assembly. Although a general mechanism of PhLP1-mediated G βγ assembly has been postulated, many of the details about this process are still missing. Structural analysis of key complexes that are important intermediates in the G βγ assembly process can generate snapshots that provide molecular details of the mechanism beyond current understanding. We have isolated two important intermediates in the assembly process, the Gβ1-CCT and PhLP1-Gβ1-CCT complexes assembled in vivo in insect cells, and have determined their structures by cryo-electron microscopy (cryo-EM). Structural analysis reveals that Gβ1, representing the WD40 repeat proteins which are a major class of CCT substrates, interacts specifically with the apical domain of CCTβ. Gβ1 binding experiments with several chimeric CCT subunits confirm a strong interaction of Gβ1 with CCTβ and map Gβ1 binding to α-Helix 9 and the loop between β-strands 6 and 7. These regions are part of a hydrophobic surface of the CCTβ apical domain facing the chaperonin cavity. Docking the Gβ molecule into the two 3D reconstructions (Gβ1-CCT and PhLP1-Gβ1-CCT) reveals that upon PhLP1 binding to Gβ1-CCT, the quasi-folded Gβ molecule is constricted to a more native state and shifted to an angle that can lead to the release of folded Gβ1 from CCT. Moreover, mutagenesis of the CCTβ subunit suggests that PhLP1 can interact with the tip of the apical domain of CCTβ subunit at residue S260, which is a downstream phosphorylation target site of RSK and S6K kinases from the Ras-MAPK and mTOR pathways. These results reveal a novel mechanism of PhLP1-mediated Gβ folding and its release from CCT. The next important step in testing the PhLP1-mediated Gβγ assembly hypothesis is to investigate the function of PhLP1 in vivo. We have prepared a rod-specific PhLP1 conditional knockout mouse in which the physiological consequences of the loss of PhLP1 functions have been characterized. The loss of PhLP1 has led to profound consequences on the ability of these rods to detect light as a result of a significant reduction in the expression of transducin (Gt) subunits. Expression of other G protein subunits as well as Gβ5-RGS9-1 complexes was also greatly decreased, yet all of this occurs without resulting in rapid degeneration of the photoreceptor cells. These results show for the first time the essential nature of PhLP1 for Gβγ and Gβ5-RGS dimer assembly in vivo, confirming results from cell culture and structural studies.
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Xiao, Ruoyu. "Protein disulfide isomerase : function and mechanism in oxidative protein folding /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-238-1/.

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Bruell, Christian M. "Mechanism of protein synthesis in Mycobacterium smegmatis /." Zürich : ETH, 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17733.

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Staniforth, Rosemary A. "The mechanism of chaperonin-assisted protein folding." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238915.

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Hoffman, Mary M. "Mechanism of MDR protein mediated multidrug resistance /." Access full-text from WCMC, 1997. http://proquest.umi.com/pqdweb?did=733008491&sid=6&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Hill, Donna Monique. "Mechanism of centaurin-alpha-1 control of neuronal differentiation." Birmingham, Ala. : University of Alabama at Birmingham, 2010. https://www.mhsl.uab.edu/dt/2010m/hill.pdf.

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Thesis (M.S.)--University of Alabama at Birmingham, 2009.
Title from PDF t.p. (viewed June 30, 2010). Additional advisors: Lori McMahon, Stephen Watts. Includes bibliographical references (p. 31-35).
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Lindgren, Matteus. "On the mechanism of Urea-induced protein denaturation." Doctoral thesis, Umeå universitet, Kemiska institutionen, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-33151.

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It is well known that folded proteins in water are destabilized by the addition of urea. When a protein loses its ability to perform its biological activity due to a change in its structure, it is said to denaturate. The mechanism by which urea denatures proteins has been thoroughly studied in the past but no proposed mechanism has yet been widely accepted. The topic of this thesis is the study of the mechanism of urea-induced protein denaturation, by means of Molecular Dynamics (MD) computer simulations and Nuclear Magnetic Resonance (NMR) spectroscopy. Paper I takes a thermodynamic approach to the analysis of protein – urea solution MD simulations. It is shown that the protein – solvent interaction energies decrease significantly upon the addition of urea. This is the result of a decrease in the Lennard-Jones energies, which is the MD simulation equivalent to van der Waals interactions. This effect will favor the unfolded protein state due to its higher number of protein - solvent contacts. In Paper II, we show that a combination of NMR spin relaxation experiments and MD simulations can successfully be used to study urea in the protein solvation shell. The urea molecule was found to be dynamic, which indicates that no specific binding sites exist. In contrast to the thermodynamic approach in Paper I, in Paper III we utilize MD simulations to analyze the affect of urea on the kinetics of local processes in proteins. Urea is found to passively unfold proteins by decreasing the refolding rate of local parts of the protein that have unfolded by thermal fluctuations. Based upon the results of Paper I – III and previous studies in the field, I propose a mechanism in which urea denatures proteins mainly by an enthalpic driving force due to attractive van der Waals interactions. Urea interacts favorably with all the different parts of the protein. The greater solvent accessibility of the unfolded protein is ultimately the factor that causes unfolded protein structures to be favored in concentrated urea solutions.
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Hanazono, Yuya. "Structural studies on the mechanism of protein folding." 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/188506.

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Books on the topic "Protein mechanism"

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Mechanism in protein chemistry. New York: Garland Pub., 1995.

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Structure and mechanism in protein science: A guide to enzyme catalysis and protein folding. New York: W.H. Freeman, 1999.

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Vitiello, Christal Lourdes. Mechanism of Transcription Arrest By The Nun Protein of Bacteriophage HK022. [New York, N.Y.?]: [publisher not identified], 2012.

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Landini, Paolo. Mechanism of transcription activation by the Ada protein of Escherichia coli. Birmingham: University of Birmingham, 1999.

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Kozik, Andrzej. Thiamine-protein interaction: Chemical mechanism of ligand-binding and bioanalytical application of thiamine-binding proteins from seeds. Kraków: Nakł. Uniwersytetu Jagiellońskiego, 1996.

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Cruickshank, Jennifer. The DNA binding mechanism of the Epstein-Barr origin binding protein, EBNA1. Ottawa: National Library of Canada, 1999.

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Konarski, Jakub Z. Molecular mechanism of protein kinase C enhancement of N-methyl-D-aspartate receptor calcium-dependent inactivation. Ottawa: National Library of Canada, 2002.

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Williams, Sophie I., and Christopher E. Rogers. HER2 and cancer: Mechanism, testing, and targeted therapy. New York: Nova Biomedical Books, 2011.

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Li, Zhiying. Simulated force-induced stretching of protein a[alpha}-helices: The effect of primary sequence on the unfolding mechanism. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2004.

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Frahm, Grant E. Investigation of the mechanism of transfer of a-tocopherol by the human a-tocopherol transfer protein (H-a-TTP). St. Catharines, Ont: Brock University, Centre for Biotechnology, 2007.

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Book chapters on the topic "Protein mechanism"

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Schwarz, Hans Peter, and John H. Griffin. "Mechanism of Action of Protein C." In Protein C, edited by Irene Witt, 5–18. Berlin, Boston: De Gruyter, 1985. http://dx.doi.org/10.1515/9783110852707-005.

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Suzuki, Yuichiro J. "Mechanism and Functions of Protein Decarbonylation." In Protein Carbonylation, 97–109. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781119374947.ch5.

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Travers, Andrew. "The mechanism of eukaryotic transcription." In DNA-Protein Interactions, 130–57. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1480-6_6.

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Koronakis, Vassilis, Jeyanthy Eswaran, and Colin Hughes. "The Type I Export Mechanism." In Bacterial Protein Toxins, 71–79. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817893.ch5.

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Kadowaki, Motoni, Rina Venerando, Giovanni Miotto, and Glenn E. Mortimore. "Mechanism of Autophagy in Permeabilized Hepatocytes." In Intracellular Protein Catabolism, 113–19. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0335-0_13.

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Travers, Andrew. "The mechanism of RNA chain initiation." In DNA-Protein Interactions, 87–108. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1480-6_4.

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Bartlett, P. A. "The Interplay Between Enzyme Mechanism, Protein Structure, and Inhibitor and Catalyst Design." In Protein Structure and Protein Engineering, 86–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-74173-9_10.

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Buxbaum, Engelbert. "Enzyme Kinetics and Mechanism." In Fundamentals of Protein Structure and Function, 111–40. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19920-7_5.

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Kon, Maria, and Ana Maria Cuervo. "Autophagy: An Alternative Degradation Mechanism for Misfolded Proteins." In Protein Misfolding Diseases, 113–29. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470572702.ch6.

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Shai, Yechiel. "Mechanism of Membrane Permeation and Pore Formation by Antimicrobial Peptides." In Protein-Lipid Interactions, 187–217. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527606769.ch9.

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Conference papers on the topic "Protein mechanism"

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Yang, Jingqi, and Lingyun Chen. "Effects of extraction methods on the composition, structure, and gelling mechanism of pea proteins." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/yyzj7229.

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A a systematic understanding of pea protein composition, conformation and functionalities as impacted by extraction methods is limited. Moreover, previous works focused on investigating the effects of gelling conditions on gel properties and showed that pea protein had significantly lower gelling capacity and weaker gel texture than soy proteins. However, gelling mechanism of pea protein has not been fully understood yet. Six protein isolation methods were selected, including air-classification (AC), alkaline extraction followed by isoelectric precipitation (AI) or ultrafiltration (AU), salt solution extraction followed by dialysis (SD) or ultrafiltration (SU) and micellar precipitation (MP). The pea protein compositions were analyzed by size exclusive-HPLC. The structures of proteins were revealed by Fourier-transform infrared spectrum, intrinsic fluorescence, and surface hydrophobicity. This study found that recovery methods determine the protein composition. Those obtained by ultrafiltration and dialysis contains albumins, whereas precipitation methods specifically retained globulins. Pea proteins prepared by alkaline solution had higher 11S/7S ratio and surface hydrophobicity than those by salt solution. The protein isolates by different methods showed large variation in gelling properties. Pea protein extracted by MP, AU or SU formed gels with a compressive strength of 60-80 kPa, comparable to soy protein gels. AU, SU, MP experienced high degree of unfolding upon heating, resulting in the exposure of interaction regions. The appropriate level of 7S allowed unfolded proteins to aggregate in a more organized manner through intra-floc links. These together led to homogeneous percolating-like microstructure with greater strength. Instead, the aggregates triggered by extraction through SD method prevented protein unfolding, leading to coarse particulate structure, and weak gels. This study showed the impact of extraction methods on protein composition and structure in relation to their gelling properties. The generated knowledge will help industry target the improved pea protein gels for specific applications.
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Arikawa, Keisuke. "Investigation of Algorithms for Analyzing Protein Internal Motion From Viewpoint of Robot Kinematics." In ASME 2010 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/detc2010-28551.

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We investigate various algorithms for analyzing the characteristics of the internal motion of proteins based on the analogies between their kinematic structures and robotic mechanisms. First, we introduce an artificial simple protein model, planar main chain (PMC), composed of a planar serial link mechanism to investigate the algorithms. Then, we develop algorithms for analyzing the conformational fluctuations by applying the manipulability analysis of robot manipulators and control strategies for redundant manipulators. Next, we develop algorithms for analyzing the conformational deformation caused by the external forces and to evaluate the compliances of the specified parts of proteins. Finally, we show that the proposed algorithms developed by using PMC models are applicable for the three dimensional main chain structures of real proteins, and may be used to analyze their characteristics of the internal motion. We also reveal some preliminary simulation results of the analysis of a real protein.
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Atanu, F. O., E. Oveido-Orta, and K. A. Watson. "Predicting protein transport mechanism and immune response using spatial protein motifs and epitopes." In BCB'13: ACM-BCB2013. New York, NY, USA: ACM, 2013. http://dx.doi.org/10.1145/2506583.2506656.

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Nicolau, Dan V. "Mechanism-dependent resolution for protein micro/nano-patterning." In Microlithography 2000, edited by Francis M. Houlihan. SPIE, 2000. http://dx.doi.org/10.1117/12.388330.

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Jamaluddin, Moideen P., C. Sreedevi, Ancy Thomas, and Lissy K. Krishnan. "A MOLECULAR MECHANISM FOR THE DITHI0THREIT0L-MEDIAT5D PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644495.

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Biochemical mechanisms of stimulus response coupling is an intricate problem in platelet biochemistry. Recently we obtained evidence that support the view that conformational changes of an (unsaturated fatty acid – and U46619-binding) haemoprotein induced by the binding of arachidonic acid, H2O2 or PGH2 liberated in apparently different platelet compartments in response to different stimuli could constitute a mechanism (L.K. Krishnan … M.P. Jamaluddin, FEBS Lett, in the press). We investigated the effect of dithiothreitol (DTT), a platelet agonist whose mechanism of action is unknown, on the purified haemoprotein. DTT was found by spectral measurements and gelfiltration experiments to bring about a slow time-dependent conformational .change and oligomerization of the protein concomitantly with its oxidation. Oxidised DTT (trans-4,5-dihy-droxy-1,2-dithiane) was found to induce a similar conformational change by binding to the protein (halfsaturation cancn. 2 mM). Oligomerization changed the charge characteristics of the protein, from net positive to net negative, ait pH 7.4. Protein-protein association is associated with large volume increases. Excluded volume effects and changes in charge distribution at the side of protein conformational change could trigger actin polymerization, pseudopod formation and aggregation, modulated by protein phosphorylation and Ca2+ concentration. In conformity with these ideas oxidized DTT near its half-maximal saturation concentration for the protein, was found to aggregate gelfiltered calf platelets. Presumably it functions as a thioanalogue of PGH2. Oxidized glutathione or oxidized 2-mercaptoethanol could also bring about protein conformational change and platelet aggregation.
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Pereira, Marco, John Deak, Lynn Richard, Hui-Ling Chiu, Lynn Schilling, and R. J. Dwayne Miller. "Energetics and Dynamics of Global Protein Motion." In International Conference on Ultrafast Phenomena. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/up.1992.thb4.

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Functionally important motions in biological systems requires the correlated displacement of thousands of atoms. The exact mechanism for the protein response to a stimulus for the functionally relevant motions is poorly understood. The classic models for deterministic protein motion rely on potential energy gradients that are created through the interaction with a stimulus to provide the forces that orchestrate the molecular motion. The question is over what length scale are these forces distributed and what are the magnitudes of the driving force, i.e., the energetics for the structural changes. In this regard, heme proteins provide ideal systems for addressing these issues. Photodissociation of the axial ligand at the heme site selectively triggers the functionally important structural changes involved in oxygen binding and allosteric regulation of oxygen transport in heme proteins.
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Comp, P. C., and C. T. Esmon. "Defects in the protein C pathway." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643715.

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Activated protein C functions as an anticoagulant by enzymatically degrading factors Va and Villa in the clotting cascade. Protein C may be converted to its enzymatically active form bythrombin. The rate at which thrombin cleavage of the zymogen occurs is greatly enhanced when thrombin is bound to an endothelial cell receptor protein, thrombomodulin. Activated proteinC has a relatively long half-life in vivo and the formation of activated protein C in response to low level thrombin infusion suggests that the protein C system may provide a feedback mechanism to limit blood clotting. Clinical support for such a physiologic role for activated protein C includes an increased incidence of thrombophlebitis and pulmonary emboli in heterozygous deficient individuals, and severe, often fatal, cutaneous thrombosis in homozygous deficient newborns. A third thrombotic condition associated with protein C deficiency is coumarin induced skin (tissue) necrosis. This localized skin necrosis occurs shortly after the initiation of coumarin therapy and is hypothesized to bedue to the rapid disappearance of protein C activity in the plasma beforean adequate intensity of anticoagulation is achieved. Recent estimates of heterozygous protein C deficiency range as high as 1 in 300 individuals in the general population. Since coumarin compounds are in routine clinical use throughout the world and skin necrosis remains a relatively rare clinical finding, this suggests that factors other than protein C deficiency alone may be involved in the pathogenesis of the skin necrosis.The anticoagulant properties of activated protein C are greatly enhanced by another vitamin K-dependent plasma protein, protein S. Protein S functions by increasing the affinity of activated protein C for cell surfaces.Protein S is found in two forms in plasma: free and in complex with C4b-binding protein, "an inhibitor of the complement system. Free protein S is functionally active and the complexed protein S is not active. Individuals congenitally deficient in protein S ae subject to recurrent thromboembolicevents. At least two classes of protin S deficiency occur.Some patienshavedecreased levels of protein S antigen and reduced protein S functional activity. A second group of deficient individuals have normal levels of protein S antigen but most or all their protein S is complexed to C4b-binding protein and they have little or no functional protein S activity. Such a protein S distribution could result from abnormal forms of protein S or C4b-binding protein or some other abnormal plasma or cellular component. Patients with functionally inactive forms of protein S have yet to be identified. Identification of protein S deficient individuals is complicated by thepossible effect of sex hormones on plasma protein S levels. Total protein S antigen is reduced during pregnancyand during oral contraceptive administration. This finding is of practicalclinical importance since the decrease in protein S which occurs during pregnancy may be an added risk factor for congenitally protein S deficient women and may explain why some proteinS deficient women experience their first episode of thrombosis during pregnancy.In addition to having anticoagulant properties, activated protein C enhances fibrinolysis, at least in part,by inhibiting the inhibitor of tissueplasminogen activator. This profibrinolytic effect is enhanced by protein S and cell surfaces. This protection of plasminogen activator activity suggests that the combination of tissue plasminogen activator and activated protein C may be useful in the treatment of coronary artery thrombi. Tissueplasminogen activator would promote clot lysis while activated protein C protected the plasminogen activatorfrom inhibition and also prevented further clot deposition. There is no evidence at present that fibrinolytic activity is reduced in protein C deficient individuals. The possible clinical relevance of this aspect of protein Cfunction in the predisposition of protein C deficient individuals to thrombosis remains to be defined.
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Smith, Karl J. P., Joshua Winans, and James McGrath. "Ultrathin Membrane Fouling Mechanism Transitions in Dead-End Filtration of Protein." In ASME 2016 14th International Conference on Nanochannels, Microchannels, and Minichannels collocated with the ASME 2016 Heat Transfer Summer Conference and the ASME 2016 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/icnmm2016-7989.

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Ultrathin membranes will likely see great utility in future membrane-based separations, but key aspects of the performance of these membranes, especially when they are used to filter protein, remain poorly understood. In this work we perform protein filtrations using new nanoporous silicon nitride (NPN) membranes. Several concentrations of protein are filtered using dead end filtration in a benchtop centrifuge, and we track fouling based on the amount of filtrate passed over time. A modification of the classic fouling model that includes the effects of using a centrifuge and allow for the visualization of a transition between pore constriction and cake filtration demonstrate that for a range of protein concentrations, cake filtration supersedes pore constriction after ∼30 seconds at 690 g.
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Dyer, R. Brian, and Timothy P. Causgrove. "Ultrafast Protein Relaxation: Time-Resolved Infrared Studies of Protein Dynamics Triggered by CO Photodissociation from CO Myoglobin." In International Conference on Ultrafast Phenomena. Washington, D.C.: Optica Publishing Group, 1994. http://dx.doi.org/10.1364/up.1994.tub.4.

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A critical feature of the biological function of heme proteins is the direct coupling of protein motion to the process of binding exogenous ligands to the heme. In carbonmonoxymyoglobin (MbCO), a substantial, specific conformational relaxation is associated with the transition from the ligated to the unligated form of the protein. The analogous tertiary structural changes of the monomer heme subunits of hemoglobin ultimately lead to the R→T quaternary structural transition, the allosteric control mechanism of O2 binding efficiency [1]. We have studied these processes on the earliest timescales, using picosecond, time-resolved infrared (TRIR) spectroscopy. It has long been known that infrared spectra in the amide region are sensitive to protein secondary conformation [2]. Recent advances in equipment and techniques have permitted researchers to quantitatively predict secondary structures from infrared spectra [3,4], particularly in the amide I region [4]. Therefore, it is now possible to study protein motion in time-resolved experiments on dynamics and function. The ligation reactions of small molecules such as CO with the heme site of Mb exemplify the mechanisms available to O2. CO is an ideal candidate for initial time-resolved IR experiments in the amide I region because it is easily photolyzed, little geminate recombination [5], and the structure of both MbCO and unligated Mb have been studied by crystallographic methods [6]. TRIR has already been applied to the stretching vibrations of the bound and free CO ligand [7,8]; dynamics of the protein, however, have yet to be probed by TRIR spectroscopy of the protein vibrations. Here we report results on the motions of the protein in response to ligation reactions, probed in the amide I region centered about 1650 cm-1.
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Bhutani, Garima, Pratima Verma, Kausik Chattopadhyay, and Arijit K. De. "Ultrafast Dynamics of “Reverse Protonation” in the Red Fluorescent Protein mKeima." In International Conference on Ultrafast Phenomena. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/up.2022.w4a.1.

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We investigate ultrafast dynamics of excited-state proton transfer coupled with cis-trans isomerization in the red fluorescent protein mKeima, elucidating the mechanism of “reverse protonation” and how it is fine-tuned by pH of the local environment.
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Reports on the topic "Protein mechanism"

1

Theg, Steven. Mechanism of Protein Transport on the Twin Arginine Translocation Pathway. Office of Scientific and Technical Information (OSTI), September 2018. http://dx.doi.org/10.2172/1633086.

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Rajabi, Hasan N. The Mechanism of Retinoblastoma Protein-Mediated Terminal Cell Cycle Arrest. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada421731.

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Lapidot, Moshe, and Vitaly Citovsky. molecular mechanism for the Tomato yellow leaf curl virus resistance at the ty-5 locus. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604274.bard.

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Tomato yellow leaf curl virus (TYLCV) is a major pathogen of tomato that causes extensive crop loss worldwide, including the US and Israel. Genetic resistance in the host plant is considered highly effective in the defense against viral infection in the field. Thus, the best way to reduce yield losses due to TYLCV is by breeding tomatoes resistant or tolerant to the virus. To date, only six major TYLCV-resistance loci, termed Ty-1 to Ty-6, have been characterized and mapped to the tomato genome. Among tomato TYLCV-resistant lines containing these loci, we have identified a major recessive quantitative trait locus (QTL) that was mapped to chromosome 4 and designated ty-5. Recently, we identified the gene responsible for the TYLCV resistance at the ty-5 locus as the tomato homolog of the gene encoding messenger RNA surveillance factor Pelota (Pelo). A single amino acid change in the protein is responsible for the resistant phenotype. Pelo is known to participate in the ribosome-recycling phase of protein biosynthesis. Our hypothesis was that the resistant allele of Pelo is a “loss-of-function” mutant, and inhibits or slows-down ribosome recycling. This will negatively affect viral (as well as host-plant) protein synthesis, which may result in slower infection progression. Hence we have proposed the following research objectives: Aim 1: The effect of Pelota on translation of TYLCV proteins: The goal of this objective is to test the effect Pelota may or may not have upon translation of TYLCV proteins following infection of a resistant host. Aim 2: Identify and characterize Pelota cellular localization and interaction with TYLCV proteins: The goal of this objective is to characterize the cellular localization of both Pelota alleles, the TYLCV-resistant and the susceptible allele, to see whether this localization changes following TYLCV infection, and to find out which TYLCV protein interacts with Pelota. Our results demonstrate that upon TYLCV-infection the resistant allele of pelota has a negative effect on viral replication and RNA transcription. It is also shown that pelota interacts with the viral C1 protein, which is the only viral protein essential for TYLCV replication. Following subcellular localization of C1 and Pelota it was found that both protein localize to the same subcellular compartments. This research is innovative and potentially transformative because the role of Peloin plant virus resistance is novel, and understanding its mechanism will lay the foundation for designing new antiviral protection strategies that target translation of viral proteins. BARD Report - Project 4953 Page 2
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Barash, Itamar, and Robert Rhoads. Translational Mechanisms Governing Milk Protein Levels and Composition. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7696526.bard.

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Original objectives: The long-term goal of the research is to achieve higher protein content in the milk of ruminants by modulating the translational apparatus of the mammary gland genetically, nutritionally, or pharmacologically. The short-term objectives are to obtain a better understanding of 1) the role of amino acids (AA) as regulators of translation in bovine and mouse mammary epithelial cells and 2) the mechanism responsible for the synergistic enhancement of milk-protein mRNA polyadenylation by insulin and prolactin. Background of the topic: In many cell types and tissues, individual AA affect a signaling pathway which parallels the insulin pathway to modulate rates and levels of protein synthesis. Diverse nutritional and hormonal conditions are funneled to mTOR, a multidomain serine/threonine kinase that regulates a number of components in the initiation and elongation stages of translation. The mechanism by which AA signal mTOR is largely unknown. During the current grant period, we have studied the effect of essential AA on mechanisms involved in protein synthesis in differentiated mammary epithelial cells cultured under lactogenic conditions. We also studied lactogenic hormone regulation of milk protein synthesis in differentiated mammary epithelial cells. In the first BARD grant (2000-03), we discovered a novel mechanism for mRNA-specific hormone-regulated translation, namely, that the combination of insulin plus prolactin causes cytoplasmic polyadenylation of milk protein mRNAs, which leads to their efficient translation. In the current BARD grant, we have pursued the signaling pathways of this novel hormone action. Major conclusions/solutions/achievements: The positive and negative signaling from AA to the mTOR pathway, combined with modulation of insulin sensitization, mediates the synthesis rates of total and specific milk proteins in mammary epithelial cells. The current in vitro study revealed cryptic negative effects of Lys, His, and Thr on cellular mechanisms regulating translation initiation and protein synthesis in mammary epithelial cells that could not be detected by conventional in vivo analyses. We also showed that a signaling pathway involving Jak2 and Stat5, previously shown to lead from the prolactin receptor to transcription of milk protein genes, is also used for cytoplasmic polyadenylation of milk protein mRNAs, thereby stabilizing these mRNAs and activating them for translation. Implications: In vivo, plasma AA levels are affected by nutritional and hormonal effects as well as by conditions of exercise and stress. The amplitude in plasma AA levels resembles that applied in the current in vitro study. Thus, by changing plasma AA levels in the epithelial cell microenvironment or by sensitizing the mTOR pathway to their presence, it should be possible to modulate the rate of milk protein synthesis. Furthermore, knowledge that phosphorylation of Stat5 is required for enhanced milk protein synthesis in response to lactogenic opens the possibility for pharmacologic approaches to increase the phosphorylation of Stat5 and, thereby, milk protein production.
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Epel, Bernard L., Roger N. Beachy, A. Katz, G. Kotlinzky, M. Erlanger, A. Yahalom, M. Erlanger, and J. Szecsi. Isolation and Characterization of Plasmodesmata Components by Association with Tobacco Mosaic Virus Movement Proteins Fused with the Green Fluorescent Protein from Aequorea victoria. United States Department of Agriculture, September 1999. http://dx.doi.org/10.32747/1999.7573996.bard.

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The coordination and regulation of growth and development in multicellular organisms is dependent, in part, on the controlled short and long-distance transport of signaling molecule: In plants, symplastic communication is provided by trans-wall co-axial membranous tunnels termed plasmodesmata (Pd). Plant viruses spread cell-to-cell by altering Pd. This movement scenario necessitates a targeting mechanism that delivers the virus to a Pd and a transport mechanism to move the virion or viral nucleic acid through the Pd channel. The identity of host proteins with which MP interacts, the mechanism of the targeting of the MP to the Pd and biochemical information on how Pd are alter are questions which have been dealt with during this BARD project. The research objectives of the two labs were to continue their biochemical, cellular and molecular studies of Pd composition and function by employing infectious modified clones of TMV in which MP is fused with GFP. We examined Pd composition, and studied the intra- and intercellular targeting mechanism of MP during the infection cycle. Most of the goals we set for ourselves were met. The Israeli PI and collaborators (Oparka et al., 1999) demonstrated that Pd permeability is under developmental control, that Pd in sink tissues indiscriminately traffic proteins of sizes of up to 50 kDa and that during the sink to source transition there is a substantial decrease in Pd permeability. It was shown that companion cells in source phloem tissue export proteins which traffic in phloem and which unload in sink tissue and move cell to cell. The TAU group employing MP:GFP as a fluorescence probe for optimized the procedure for Pd isolation. At least two proteins kinases found to be associated with Pd isolated from source leaves of N. benthamiana, one being a calcium dependent protein kinase. A number of proteins were microsequenced and identified. Polyclonal antibodies were generated against proteins in a purified Pd fraction. A T-7 phage display library was created and used to "biopan" for Pd genes using these antibodies. Selected isolates are being sequenced. The TAU group also examined whether the subcellular targeting of MP:GFP was dependent on processes that occurred only in the presence of the virus or whether targeting was a property indigenous to MP. Mutant non-functional movement proteins were also employed to study partial reactions. Subcellular targeting and movement were shown to be properties indigenous to MP and that these processes do not require other viral elements. The data also suggest post-translational modification of MP is required before the MP can move cell to cell. The USA group monitored the development of the infection and local movement of TMV in N. benthamiana, using viral constructs expressing GFP either fused to the MP of TMV or expressing GFP as a free protein. The fusion protein and/or the free GFP were expressed from either the movement protein subgenomic promoter or from the subgenomic promoter of the coat protein. Observations supported the hypothesis that expression from the cp sgp is regulated differently than expression from the mp sgp (Szecsi et al., 1999). Using immunocytochemistry and electron microscopy, it was determined that paired wall-appressed bodies behind the leading edge of the fluorescent ring induced by TMV-(mp)-MP:GFP contain MP:GFP and the viral replicase. These data suggest that viral spread may be a consequence of the replication process. Observation point out that expression of proteins from the mp sgp is temporary regulated, and degradation of the proteins occurs rapidly or more slowly, depending on protein stability. It is suggested that the MP contains an external degradation signal that contributes to rapid degradation of the protein even if expressed from the constitutive cp sgp. Experiments conducted to determine whether the degradation of GFP and MP:GFP was regulated at the protein or RNA level, indicated that regulation was at the protein level. RNA accumulation in infected protoplast was not always in correlation with protein accumulation, indicating that other mechanisms together with RNA production determine the final intensity and stability of the fluorescent proteins.
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Lazarus, Rachel C. Protein Modification: A Proposed Mechanism for the Long-Term Pathogenesis of Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, May 2015. http://dx.doi.org/10.21236/ad1012716.

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Gafni, Yedidya, and Vitaly Citovsky. Molecular interactions of TYLCV capsid protein during assembly of viral particles. United States Department of Agriculture, April 2007. http://dx.doi.org/10.32747/2007.7587233.bard.

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Tomato yellow leaf curl geminivirus (TYLCV) is a major pathogen of cultivated tomato, causing up to 100% crop loss in many parts of the world. The present proposal, a continuation of a BARD-funded project, expanded our understanding of the molecular mechanisms by which CP molecules, as well as its pre-coat partner V2, interact with each other (CP), with the viral genome, and with cellular proteins during assembly and movement of the infectious virions. Specifically, two major objectives were proposed: I. To study in detail the molecular interactions between CP molecules and between CP and ssDNA leading to assembly of infectious TYLCV virions. II. To study the roles of host cell factors in TYLCV assembly. Our research toward these goals has produced the following major achievements: • Characterization of the CP nuclear shuttling interactor, karyopherin alpha 1, its pattern of expression and the putative involvement of auxin in regulation of its expression. (#1 in our list of publication, Mizrachy, Dabush et al. 2004). • Identify a single amino acid in the capsid protein’s sequence that is critical for normal virus life-cycle. (#2 in our list of publications, Yaakov, Levy et al. in preparation). • Development of monoclonal antibodies with high specificity to the capsid protein of TYLCV. (#3 in our list of publications, Solmensky, Zrachya et al. in press). • Generation of Tomato plants resistant to TYLCV by expressing transgene coding for siRNA targeted at the TYLCV CP. (#4 in our list of publications, Zrachya, Kumar et al. in press). •These research findings provided significant insights into (i) the molecular interactions of TYLCV capsid protein with the host cell nuclear shuttling receptor, and (ii) the mechanism by which TYLCV V2 is involved in the silencing of PTGS and contributes to the virus pathogenicity effect. Furthermore, the obtained knowledge helped us to develop specific strategies to attenuate TYLCV infection, for example, by blocking viral entry into and/or exit out of the host cell nucleus via siRNA as we showed in our publication recently (# 4 in our list of publications). Finally, in addition to the study of TYLCV nuclear import and export, our research contributed to our understanding of general mechanisms for nucleocytoplasmic shuttling of proteins and nucleic acids in plant cells. Also integration for stable transformation of ssDNA mediated by our model pathogen Agrobacterium tumefaciens led to identification of plant specific proteins involved.
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Sela, Shlomo, and Michael McClelland. Investigation of a new mechanism of desiccation-stress tolerance in Salmonella. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598155.bard.

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Low-moisture foods (LMF) are increasingly involved in foodborne illness. While bacteria cannot grow in LMF due to the low water content, pathogens such as Salmonella can still survive in dry foods and pose health risks to consumer. We recently found that Salmonella secretes a proteinaceous compound during desiccation, which we identified as OsmY, an osmotic stress response protein of 177 amino acids. To elucidate the role of OsmY in conferring tolerance against desiccation and other stresses in Salmonella entericaserovarTyphimurium (STm), our specific objectives were: (1) Characterize the involvement of OsmY in desiccation tolerance; (2) Perform structure-function analysis of OsmY; (3) Study OsmY expression under various growth- and environmental conditions of relevance to agriculture; (4) Examine the involvement of OsmY in response to other stresses of relevance to agriculture; and (5) Elucidate regulatory pathways involved in controlling osmY expression. We demonstrated that an osmY-mutant strain is impaired in both desiccation tolerance (DT) and in long-term persistence during cold storage (LTP). Genetic complementation and addition of a recombinantOsmY (rOsmY) restored the mutant survival back to that of the wild type (wt). To analyze the function of specific domains we have generated a recombinantOsmY (rOsmY) protein. A dose-response DT study showed that rOsmY has the highest protection at a concentration of 0.5 nM. This effect was protein- specific as a comparable amount of bovine serum albumin, an unrelated protein, had a three-time lower protection level. Further characterization of OsmY revealed that the protein has a surfactant activity and is involved in swarming motility. OsmY was shown to facilitate biofilm formation during dehydration but not during bacterial growth under optimal growth conditions. This finding suggests that expression and secretion of OsmY under stress conditions was potentially associated with facilitating biofilm production. OsmY contains two conserved BON domains. To better understand the role of the BON sites in OsmY-mediated dehydration tolerance, we have generated two additional rOsmY constructs, lacking either BON1 or BON2 sites. BON1-minus (but not BON2) protein has decreased dehydration tolerance compared to intact rOsmY, suggesting that BON1 is required for maximal OsmY-mediated activity. Addition of BON1-peptide at concentration below 0.4 µM did not affect STm survival. Interestingly, a toxic effect of BON1 peptide was observed in concentration as low as 0.4 µM. Higher concentrations resulted in complete abrogation of the rOsmY effect, supporting the notion that BON-mediated interaction is essential for rOsmY activity. We performed extensive analysis of RNA expression of STm undergoing desiccation after exponential and stationary growth, identifying all categories of genes that are differentially expressed during this process. We also performed massively in-parallel screening of all genes in which mutation caused changes in fitness during drying, identifying over 400 such genes, which are now undergoing confirmation. As expected OsmY is one of these genes. In conclusion, this is the first study to identify that OsmY protein secreted during dehydration contributes to desiccation tolerance in Salmonella by facilitating dehydration- mediated biofilm formation. Expression of OsmY also enhances swarming motility, apparently through its surfactant activity. The BON1 domain is required for full OsmY activity, demonstrating a potential intervention to reduce pathogen survival in food processing. Expression and fitness screens have begun to elucidate the processes of desiccation, with the potential to uncover additional specific targets for efforts to mitigate pathogen survival in desiccation.
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So, Joanne D. An Essential Protein Repair Enzyme: Investigation of the Molecular Recognition Mechanism of Methionine Sulfoxide Reductase A. Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada485775.

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Citovsky, Vitaly, and Yedidya Gafni. Suppression of RNA Silencing by TYLCV During Viral Infection. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7592126.bard.

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The Israeli isolate of Tomato yellow leaf curl geminivirus (TYLCV-Is) is a major tomato pathogen, causing extensive (up to 100%) crop losses in Israel and in the south-eastern U.S. (e.g., Georgia, Florida). Surprisingly, however, little is known about the molecular mechanisms of TYLCV-Is interactions with tomato cells. In the current BARD project, we have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing, and showed that V2 interacts with the tomato (L. esculentum) member of the SGS3 (LeSGS3) protein family known to be involved in RNA silencing. This proposal will use our data as a foundation to study one of the most intriguing, yet poorly understood, aspects of TYLCV-Is interactions with its host plants – possible involvement of the host innate immune system, i.e., RNA silencing, in plant defense against TYLCV-Is and the molecular pathway(s) by which TYLCV-Is may counter this defense. Our project sought two objectives: I. Study of the roles of RNA silencing and its suppression by V2 in TYLCV-Is infection of tomato plants. II. Study of the mechanism by which V2 suppresses RNA silencing. Our research towards these goals has produced the following main achievements: • Identification and characterization of TYLCV V2 protein as a suppressor of RNA silencing. (#1 in the list of publications). • Characterization of the V2 protein as a cytoplasmic protein interacting with the plant protein SlSGS3 and localized mainly in specific, not yet identified, bodies. (#2 in the list of publications). • Development of new tools to study subcellular localization of interacting proteins (#3 in the list of publications). • Characterization of TYLCV V2 as a F-BOX protein and its possible role in target protein(s) degradation. • Characterization of TYLCV V2 interaction with a tomato cystein protease that acts as an anti-viral agent. These research findings provided significant insights into (I) the suppression of RNA silencing executed by the TYLCV V2 protein and (II) characterization some parts of the mechanism(s) involved in this suppression. The obtained knowledge will help to develop specific strategies to attenuate TYLCV infection, for example, by blocking the activity of the viral suppressor of gene silencing thus enabling the host cell silencing machinery combat the virus.
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