Bibliografías temáticas / Specific protein

Literatura académica sobre el tema "Specific protein"

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Publicado: 25 de mayo de 2024

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Artículos de revistas sobre el tema "Specific protein"

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Sear, Richard P. "Specific protein–protein binding in many-component mixtures of proteins". Physical Biology 1, n.º 2 (29 de abril de 2004): 53–60. http://dx.doi.org/10.1088/1478-3967/1/2/001.

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Hunte, C. "Specific protein–lipid interactions in membrane proteins". Biochemical Society Transactions 33, n.º 5 (1 de octubre de 2005): 938. http://dx.doi.org/10.1042/bst20050938.

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Hunte, C. "Specific protein–lipid interactions in membrane proteins". Biochemical Society Transactions 33, n.º 5 (26 de octubre de 2005): 938–42. http://dx.doi.org/10.1042/bst0330938.

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Many membrane proteins selectively bind defined lipid species. This specificity has an impact on correct insertion, folding, structural integrity and full functionality of the protein. How are these different tasks achieved? Recent advances in structural research of membrane proteins provide new information about specific protein–lipid interactions. Tightly bound lipids in membrane protein structures are described and general principles of the binding interactions are deduced. Lipid binding is stabilized by multiple non-covalent interactions from protein residues to lipid head groups and hydrophobic tails. Distinct lipid-binding motifs have been identified for lipids with defined head groups in membrane protein structures. The stabilizing interactions differ between the electropositive and electronegative membrane sides. The importance of lipid binding for vertical positioning and tight integration of proteins in the membrane, for assembly and stabilization of oligomeric and multisubunit complexes, for supercomplexes, as well as for functional roles are pointed out.
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Baldrich, Marcus y Werner Goebel. "Rapid and efficient site-specific mutagenesis". "Protein Engineering, Design and Selection" 3, n.º 6 (1990): 563. http://dx.doi.org/10.1093/protein/3.6.563.

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Parsons, Helen L., John C. Earnshaw, Jane Wilton, Kevin S. Johnson, Paula A. Schueler, Walt Mahoney y John McCafferty. "Directing phage selections towards specific epitopes". "Protein Engineering, Design and Selection" 9, n.º 11 (1996): 1043–49. http://dx.doi.org/10.1093/protein/9.11.1043.

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Jongen-Rêlo, Ana L. y Joram Feldon. "Specific neuronal protein". Physiology & Behavior 76, n.º 4-5 (agosto de 2002): 449–56. http://dx.doi.org/10.1016/s0031-9384(02)00732-1.

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Prasad Bahadur, Ranjit, Pinak Chakrabarti, Francis Rodier y Joël Janin. "A Dissection of Specific and Non-specific Protein–Protein Interfaces". Journal of Molecular Biology 336, n.º 4 (febrero de 2004): 943–55. http://dx.doi.org/10.1016/j.jmb.2003.12.073.

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Kusakabe, Takahiro, Kiyohisa Motoki, Yasushi Sugimoto, Yozo Takasaki y Katsuji Hori. "Human aldolase B: liver-specific properties of the isozyme depend on type B isozyme group-specific sequences". "Protein Engineering, Design and Selection" 7, n.º 11 (1994): 1387–93. http://dx.doi.org/10.1093/protein/7.11.1387.

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Tindbaek, Nikolaj, Allan Svendsen, Peter Rahbek Oestergaard y Henriette Draborg. "Engineering a substrate‐specific cold‐adapted subtilisin". Protein Engineering, Design and Selection 17, n.º 2 (febrero de 2004): 149–56. http://dx.doi.org/10.1093/protein/gzh019.

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Kumar, Challa V., Apinya Buranaprapuk y Jyotsna Thota. "Protein scissors: Photocleavage of proteins at specific locations". Journal of Chemical Sciences 114, n.º 6 (diciembre de 2002): 579–92. http://dx.doi.org/10.1007/bf02708852.

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Tesis sobre el tema "Specific protein"

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Rubin, Jonathan. "Ion-specific and water-mediated effects on protein physical stability". Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/47587.

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Protein aggregation and physical stability are perpetual concerns in medicine and industry. Misfolded protein can form ordered protein aggregates, amyloids, which are associated with a host of neurodegenerative diseases in mammals and control heritable traits in fungi and yeast. Industrially, amorphous aggregates reduce the efficacy of protein-based therapeutics and activity of enzymes during production and storage. This work studies ion-specific and solvent-based effects on protein physical stability. We show that ion-specificity significantly affects amyloid formation kinetics, aggregate morphology, thermostability, frangibility, and, most intriguingly, prion infectivity in vivo. Forming amyloid in chaotropic or kosmotropic solutions generates predominately weak or strong prion variants, respectively. Ion-specific effects also influenced amorphous aggregation of model proteins and antibodies. To quantify protein - protein stability/affinity, we developed a rapid and reliable diffusion-based technique. Our technique was able to resolve relative differences in colloidal stability between various saline and saccharide solutions. In all, this dissertation expands our understanding of ion-specific and water-mediated interactions with prion proteins and protein dispersions.
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Guelev, Vladimir Metodiev. "Peptide-based polyintercalators as sequence-specific DNA binding agents /". Full text (PDF) from UMI/Dissertation Abstracts International, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3008346.

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Davies, Holly Gibs. "MSY4, a sequence-specific RNA binding protein expressed during mouse spermatogenesis /". Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/10307.

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Lucas, Olivier. "Molecular and systemic functions of the vertebrate-specific TATA-binding protein N terminus". Diss., Montana State University, 2009. http://etd.lib.montana.edu/etd/2009/lucas/LucasO0509.pdf.

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Rossi, Merja. "Investigating cell type specific metabolism using GFP as a reporter protein". Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:0c418362-63e7-496d-9ff6-584a0c54c127.

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Metabolic flux analysis (MFA) is a powerful technique for quantifying the intracellular fluxes in central carbon metabolism. It relies on detection of stable isotope labelling from metabolites such as amino acids derived from protein. Current standard techniques are, however, unable to distinguish between different cell types in heterogeneous tissue. The aim of the thesis was to address this problem by developing and validating a strategy using green fluorescent protein (GFP) with cell type specific expression as a reporter protein for investigating the fluxes in specific cell types in the Arabidopsis thaliana root. The fundamental difficulty in applying a reporter protein strategy in a multicellular organism arises from the limited amount of recombinant protein expressed by the cells. The main novel contributions of the work in this thesis are threefold. First, a robust protocol for purification of GFP from the roots of Arabidopsis seedlings and for detection of reliable mass isotopomer distributions from the amino acids derived from GFP are described. Secondly, the reporter protein strategy is validated in this biological system with a focus on showing the data obtained by the use of the reporter protein is equal to that normally obtained from the total protein fraction. To expand on this, stable isotope labelling in isolated root hair cells is explored. These cells are easily isolated and show potential as a model system for cell type specific metabolism. Finally, the experimental data provide evidence for the feasibility of measuring data from specific cell types with appropriate mass spectrometric techniques. Analysis of cell type specific gene expression in this system suggests differences in the primary metabolism of different cell types cannot be ruled out without further investigation. Based on small scale in silico modelling described in this thesis, new solutions capable of providing data on sub-populations of cells are required, if central metabolism of the cell types differs significantly.
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Berkes, Charlotte Amelia. "Elucidating the mechanisms by which MyoD establishes muscle-specific gene expression /". Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/5071.

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Xiong, Xiaoquan. "Pancreatic islet-specific overexpression of reg3β protein". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107823.

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Reg family proteins have been implicated in islet β-cell proliferation, survival, and regeneration. Reg3β (pancreatitis-associated protein, PAP; or gene expressed in hepatocellular carcinoma-intestine-pancreas, HIP) was first reported as a pancreatic secretory protein expressed in acinar cells during the acute phase of pancreatitis. Previous studies in Dr. Liu's and other research groups have demonstrated that Reg3β was specifically induced either during islet hyperplasia in the IGF-I-deficient pancreas or as a result of GLP-1-induced islet cell growth. Reg3β has been shown to play anti-apoptotic and anti-inflammatory roles during acute pancreatitis. In the present study, we generated transgenic mice with pancreatic β-cell-specific over-expression of Reg3β and investigated the effect of Reg3β in the regulation of β-cell function during streptozotocin (STZ)-induced type 1 diabetes (T1D) and diet-induced type 2 diabetes (T2D). The data presented in Chapter II demonstrated that pancreatic islet-specific overexpression of Reg3β protein protected mice from STZ-induced T1D. The RIP-I/Reg3β mice were indistinguishable from wild-type littermates in fertility, islet morphology, β-cell mass, and insulin secretion response, yet were slightly high in glucose and low in the expression of Glut2 and insulin. These transgenic mice were significantly protected from STZ-induced hyperglycemia and weight loss that were observed in the wild-type controls. To identify the molecular networks that Reg3β is involved in, a whole genome DNA microarray analysis of isolated islet RNA samples revealed more than 45 genes whose expression were markedly up- or down-regulated as a consequence of Reg3β overexpression. We further confirmed the change in several genes, including the upregulation of islet-protective osteopontin/Spp1 and acute responsive nuclear protein Nupr1/p8 by real-time PCR, Western blots and histology. These results support the potential of Reg3β in preventing STZ-induced damage by regulating expression of specific genes.In Chapter III, mice carrying Reg3β over-expression displayed worsened T2D induced by high-fat diet (HFD), as characterized by faster and more severe development of hyperglycemia, glucose intolerance and insulin resistance. Reg3β seems to exert two opposite actions in respone to HFD: further diminishing the expression of insulin and Glut2 induced by HFD, while suppressing AMPK activity and increasing p8 expression to compensate for the loss of β-cell function. Taken together, Reg3β is a putative protector that prevents STZ-induced acute damage, but unlikely an islet growth factor and unable to protect β-cells against HFD-induced T2D. The protective effect of Reg3β is likely triggered by acute stress but ineffective against chronic stress induced by HFD.
Les protéines de la famille Reg sont impliquées dans la prolifération, la survie et la régénération des cellules pancréatiques β. Reg3β [aussi connue sous le nom de PAP (protéine associée à la pancréatite) ou encore HIP (gène exprimé dans le carcinome hépatocellulaire de l'intestin et du pancréas)] a été identifiée comme étant une protéine sécrétrice du pancréas et elle est exprimée dans les cellules acineuses pendant la phase aiguë de la pancréatite. Des études antérieures dans le laboratoire du Dr Liu ont démontré que la protéine Reg3β est spécifiquement induite durant l'hyperplasie des îlots pancréatiques à la suite d'un déficit de l'IGF-I ou encore à la suite d'une croissance de cellules d'îlots induite par GLP-I. Reg3β joue un rôle anti-apoptotique et anti-inflammatoire pendant la pancréatite aiguë. Dans cette étude, nous avons généré des souris transgéniques qui surexpriment Reg3β spécifiquement dans les cellules pancréatiques β afin d'étudier l'effet de Reg3β dans la régulation de la fonction des cellules β lors du diabète de type 1 (DT1) induit par la streptozotocine (STZ) ainsi que dans le cas du diabète de type 2 (DT2) induit par un régime alimentaire riche en gras. Les données présentées dans le chapitre II ont démontré que les îlots pancréatiques qui surexpriment la protéine murine Reg3β sont protégés du DT1 induit par la STZ. Les souris RIP-I/Reg3β transgéniques sont indiscernables des souris de contrôle de type sauvage en ce qui a trait à la fécondité, la morphologie des îlots, la masse des cellules β et la sécrétion de l'insuline. Cependant, une légère hyperglycémie et une faible expression de GLUT2 et de l'insuline ont été observées. Ces souris transgéniques sont considérablement protégées contre l'hyperglycémie induite par STZ et contre la perte de poids. A l'aide de puces d'ADN, une analyse d'échantillons d'ARN purifiés à partir d'îlots isolés a révélé l'existence de plus de 45 gènes dont l'expression est affectée par la surexpression de Reg3β. Nous avons également confirmé le changement d'expression de plusieurs gènes, y compris la régulation positive de l'osteopontin/SPP1 (qui protège les îlots et de la protéine nucléaire réactive aiguë p8/NUPR1) en utilisant le PCR en temps réel, le Western blot et l'histologie. Ces résultats confirment le potentiel de Reg3β dans la prévention des dommages induits par STZ en régulant l'expression de gènes spécifiques. Au chapitre III, nous avons démontré que la surexpression de Reg3β aggrave le DT2 induit par une alimentation riche en matières grasses. Ceci est caractérisé par le développement plus rapide et plus sévère de l'hyperglycémie, l'intolérance au glucose et la résistance à l'insuline. Reg3β semble exercer deux actions opposées en réponse à une diète riche en gras: 1) diminution accrue de l'expression basale de l'insuline et Glut2 et 2) suppression de l'activité de l'AMPK et augmentation de l'expression de la protéine p8 afin de compenser pour la perte de la fonction des cellules β. En résumé, Reg3β est un protecteur potentiel qui empêche les dommages induits par STZ aiguë, mais il est peu probable que ce soit un facteur de croissance des îlots pancréatiques. De plus, Reg3β est incapable de protéger les cellules β contre le DT2 induit par un régime alimentaire riche en gras. L'effet protecteur de Reg3β survient probablement en réponse au stress aigu mais il est inefficace contre le stress chronique induit par un régime alimentaire riche en gras.
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Giorgini, Flaviano. "Functional analysis of the murine sequence-specific RNA binding protein MSY4 /". Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/10293.

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Hussain, Maruf Ali. "Non-specific protein interactions at model chromatographic surfaces". Thesis, University of Nottingham, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243403.

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Beiersdorfer, Alex. "Site-specific Regulation of Myosin Binding Protein-C". University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1511856330493573.

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Libros sobre el tema "Specific protein"

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Gautier, Arnaud y Marlon J. Hinner, eds. Site-Specific Protein Labeling. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2272-7.

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Goebel, C. J. Protein values of specific grasses adapted to Lesotho. Maseru, Lesotho: The Division, 1986.

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Steitz, Thomas A. Structural studies of protein-nucleic acid interaction: Thesources of sequence-specific binding. Cambridge: Cambridge University Press, 1993.

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International Symposium on Site-Directed Mutagenesis and Protein Engineering (1990 Tromsø, Norway). Site-directed mutagenesis and protein engineering: Proceedings of the International Symposium on Site-Directed Mutagensis and Protein Engineering, Tromsø, 27-30 August 1990. Editado por el-Gewely M. Rafaat. Amsterdam: Elsevier Science Publishers., 1991.

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International Symposium on Site-Directed Mutagenesis and Protein Engineering (1990 Tromsø, Norway). Site-directed mutagenesis and protein engineering: Proceedings of the International Symposium on Site-Directed Mutagenesis and Protein Engineering, Tromsø, 27-30 August 1990. Editado por El-Gewely M. Rafaat. Amsterdam: Elsevier Science Publishers, 1991.

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Steitz, Thomas A. Structural studies of protein-nucleic acid interaction: The sources of sequence-specific binding. New York, NY, USA: Cambridge University Press, 1993.

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Gonzalez-Santos, Juana Maria. Characterization of the human U4/U6 specific splicing protein Hprp3p. Ottawa: National Library of Canada, 2002.

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A, Cooke Brian, King R. J. B y Molen, H. J. van der., eds. Hormones and their actions, part II: Specific actions of protein hormones. Amsterdam: Elsevier, 1988.

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Oliver, Antony William. The interaction of bacteriophage fd gene 5 protein with specific nucleic acid sequences. Portsmouth: University of Portsmouth, School of Biological Sciences, 1997.

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Hammond, Ester Mary. Apoptosis specific protein: A link between yeast autophagy and eukaryotic intermediate filament collapse. Birmingham: University of Birmingham, 1997.

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Capítulos de libros sobre el tema "Specific protein"

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Matern, Julian C. J., Anne-Lena Bachmann, Ilka V. Thiel, Gerrit Volkmann, Alexandra Wasmuth, Jens Binschik y Henning D. Mootz. "Ligation of Synthetic Peptides to Proteins Using Semisynthetic Protein trans-Splicing". En Site-Specific Protein Labeling, 129–43. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_9.

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Griffin, B. Albert, Stephen R. Adams y Roger Y. Tsien. "How FlAsH Got Its Sparkle: Historical Recollections of the Biarsenical-Tetracysteine Tag". En Site-Specific Protein Labeling, 1–6. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_1.

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Bachmann, Anne-Lena, Julian C. J. Matern, Vivien Schütz y Henning D. Mootz. "Chemical-Tag Labeling of Proteins Using Fully Recombinant Split Inteins". En Site-Specific Protein Labeling, 145–59. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_10.

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Zhao, Bo, Keya Zhang, Karan Bhuripanyo, Yiyang Wang, Han Zhou, Mengnan Zhang y Jun Yin. "Phage Selection Assisted by Sfp Phosphopantetheinyl Transferase-Catalyzed Site-Specific Protein Labeling". En Site-Specific Protein Labeling, 161–70. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_11.

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Fairhead, Michael y Mark Howarth. "Site-Specific Biotinylation of Purified Proteins Using BirA". En Site-Specific Protein Labeling, 171–84. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_12.

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Popp, Maximilian Wei-Lin. "Site-Specific Labeling of Proteins via Sortase: Protocols for the Molecular Biologist". En Site-Specific Protein Labeling, 185–98. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_13.

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Landgraf, Peter, Elmer R. Antileo, Erin M. Schuman y Daniela C. Dieterich. "BONCAT: Metabolic Labeling, Click Chemistry, and Affinity Purification of Newly Synthesized Proteomes". En Site-Specific Protein Labeling, 199–215. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_14.

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Lang, Kathrin, Lloyd Davis y Jason W. Chin. "Genetic Encoding of Unnatural Amino Acids for Labeling Proteins". En Site-Specific Protein Labeling, 217–28. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_15.

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Tamura, Tomonori y Itaru Hamachi. "Labeling Proteins by Affinity-Guided DMAP Chemistry". En Site-Specific Protein Labeling, 229–42. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_16.

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Tsukiji, Shinya y Itaru Hamachi. "Ligand-Directed Tosyl Chemistry for Selective Native Protein Labeling In Vitro, In Cells, and In Vivo". En Site-Specific Protein Labeling, 243–63. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2272-7_17.

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Actas de conferencias sobre el tema "Specific protein"

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Rahman, M. y M. Mahmoudi. "Disease specific protein corona". En SPIE BiOS, editado por Wolfgang J. Parak, Marek Osinski y Xing-Jie Liang. SPIE, 2015. http://dx.doi.org/10.1117/12.2079771.

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NARIAI, NAOKI y SIMON KASIF. "CONTEXT SPECIFIC PROTEIN FUNCTION PREDICTION". En Proceedings of the 7th Annual International Workshop on Bioinformatics and Systems Biology (IBSB 2007). IMPERIAL COLLEGE PRESS, 2007. http://dx.doi.org/10.1142/9781860949920_0017.

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Xue, Li C., Rafael A. Jordan, Yasser El-Manzalawy, Drena Dobbs y Vasant Honavar. "Ranking docked models of protein-protein complexes using predicted partner-specific protein-protein interfaces". En the 2nd ACM Conference. New York, New York, USA: ACM Press, 2011. http://dx.doi.org/10.1145/2147805.2147866.

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Krul, Elaine. "Nitrogen to Protein Conversion Factors - An update and practical guidance for their use and for determining specific factors for novel protein sources". En 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/amwx7627.

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Protein content in food is measured indirectly (since the 1880’s) by determining nitrogen (N) and using a nitrogen to protein conversion factor (NPCF). NPCFs were initially based on proteins that were readily available at the time and found to contain about 16% N. Hence, a NPCF of 6.25 (100/16) was applied to all proteins, assuming all N was from amino acids (AAs). Recent technological advances revealed differences in AA composition and content of non-protein N between proteins indicating that an NPCF of 6.25 overestimates the protein content of most foods. However, 6.25 is still widely used. In 2017, use of specific NPCFs for proteins received attention from the Codex Committee on Nutrition and Foods for Special Dietary Uses (CCNFSDU) as they addressed standards for infant and follow-up formula. Should proposed specific NPCFs for soy protein of 5.71 (proposed in 1931 based on the AA composition of glycinin) and 6.38 for dairy protein (based on unique methods of determining NPCFs) be used? In July 2019, a joint FAO/WHO Expert Meeting on Nutrition (JEMNU) systematically analyzed all data and developed a recommendation. The JEMNU report concluded that there were shortcomings of methods used for protein estimation resulting in low to moderate confidence of the factors recommended: NPCFs of 6.1 and 5.7 for dairy and soy protein, respectively. A September 2021 CCNFSDU report concluded that the NPCF value for 6.25 should be retained based on the low confidence of NPCFs recommended by JEMNU and the significant ramifications of changing the NPCFs. This highlights the challenges faced with determining the protein content for novel proteins. There are published, unstandardized methods for determining NPCFs and if the limitations of these methods are recognized and reported, this can allow data-based comparisons of NPCFs between proteins. Ideally, a universal direct method of protein content determination is needed.
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Preissner, K. T., E. Anders y G. Müller-Berghaus. "INTERACTION OF S PROTEIN/VITRONECTIN WITH CULTURED ENDOTHELIAL CELLS: PROMOTION OF ATTACHMENT AND SPECIFIC BINDING". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643635.

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The interaction of the complement inhibitor S protein, which is identical to the serum spreading factor, vitronectin, with cultured human endothelial cells of macro- and microvas- cular origin was investigated. Purified S protein, coated for 2 h on polystyrene petri dishes, induced concentration- and time-dependent attachment and spreading of human umbilical vein endothelial cells (HUVEC) as well as human omental tissqe microvasular endothelial cells (HOTMEC) at 37°C. With 3 × 105 cells/ml (final concentration) more than 50% of the cells attached within 2 h incubation at 0.3 - 3 μg/ml S protein. The effect of S protein was specific, since only monospecific antibodies against S protein prevented attachment of cells, while antibodies against fibronectin, fibrinogen or von Wille-brand factor were uneffective. The pentapeptide Gly-Arg-Gly-Asp-Ser, which contains the cell-attachment site of these adhesive proteins including S protein, inhibited the activity of S protein to promote attachment of endothelial cells in a concentration-dependent fashion; at 200 μM peptide, less than 10% of the cells became attached. Direct binding of S protein to HUVEC and HOTMEC was studied with cells in suspension at a concentration of 1 × 106 cells/ml in the presence of 1% (w/v) human serum albumin and 1 mM CaCl2 and was maximal after 120 min. Both cell types bound S protein in a concentration-dependent fashion with an estimated dissociation constant KD=0.2pM. More than 80% of bound radiolabelled S protein was displaced by unlabelled S protein, whereas binding was reduced to about 50% by the addition in excess of either fibronectin, fibrinogen, von Willebrand factor or the pentapeptide. These findings provide evidence for the specific association of S protein with endothelial cells, ultimately leading to attachment and spreading of cells. Although the promotion of attachment was highly specific for S protein, other adhesive proteins than S protein, also known to associate with endothelial cells, may in part compete with direct S protein binding.
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6

Huan, Jun, Wei Wang, Deepak Bandyopadhyay, Jack Snoeyink, Jan Prins y Alexander Tropsha. "Mining protein family specific residue packing patterns from protein structure graphs". En the eighth annual international conference. New York, New York, USA: ACM Press, 2004. http://dx.doi.org/10.1145/974614.974655.

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Ma, D. y L. Zhang. "SAT0393 Protein fingerprinting screening specific proteins in serum of patients with ankylosing spondylitis". En Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3342.

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Celik, Haydar, Jenny Han, Sung-Hyeok Hong, Gulay Bulut, Jeffrey Toretsky y Aykut Uren. "Abstract 3979: NSC305787 inhibits specific protein–protein interactions involving ezrin in osteosarcoma cells". En Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3979.

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Pedrazzini, Emanuela. "Protein-specific induction of the unfolded protein response by two maize gamma-zeins". En ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1383050.

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Ashok Kumar, A., Margaret Insley, Jay Gambee, Sharon J. Busby y Kathleen L. Berkner. "SITE SPECIFIC MUTAGENESIS WITHIN THE GLA-DOMAIN OF HUMAN FACTOR IX". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644079.

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Factor IX, a plasma protein, plays a critical role in blood coagulation. The biological activity of factor IX as well as several other plasma proteins depends on the presence of gamma-carboxy glutamic acid (Gla) residues in their amino terminal region. In vitro mutagenesis has been used to selectively replace Gla residues of factor IX with aspartic acid (Asp) residues in order to establish the contribution of individual as well as paired Gla residues to the normal functioning of the protein. These substitutions were made at positions 7, 15, 20 and 26 in human factor IX. In addition, residue number 18, a cysteine has been changed to serine in an attempt to disrupt the highly conserved disulfide bond in the gla-domain. The gla-domain mutants will be produced in mammalian cells and compared with native recombinant factor IX. A rapid immunoaffinity purification procedure, which has been used to obtain recombinant factor IX produced in the presence or absence of vitamin K, is being used to purify the mutants. Protein sequence analysis has been used to confirm complete processing and proper gamma-carboxylation of recombinant factor IX. The properties of these mutants as compared to human factor IX will be discussed.
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Informes sobre el tema "Specific protein"

1

Pang, Shen. Identification of a Protein for Prostate-Specific Infection. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 2007. http://dx.doi.org/10.21236/ada491595.

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Pang, Shen. Identification of a Protein for Prostate-Specific Infection. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 2004. http://dx.doi.org/10.21236/ada446372.

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Pang, Shen. Identification of a Protein for Prostate-Specific Infection. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 2006. http://dx.doi.org/10.21236/ada466677.

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Somerville, Ronald L. Novel Approaches to the Characterization of Specific Protein-Protein Interactions Important in Gene Expression. Fort Belvoir, VA: Defense Technical Information Center, octubre de 1994. http://dx.doi.org/10.21236/ada300480.

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Somerville, Ronald L. Novel Approaches to the Characterization of Specific Protein-Protein Interactions Important in Gene Expression. Fort Belvoir, VA: Defense Technical Information Center, octubre de 1995. http://dx.doi.org/10.21236/ada300572.

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Chen, Shu G. Characterization of Antibody Specific for Disease Associated Prion Protein. Fort Belvoir, VA: Defense Technical Information Center, julio de 2004. http://dx.doi.org/10.21236/ada432993.

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Eaton-Rye, Dr., Julian y Gaozhong Shen. Specific mutagenesis of a chlorophyll-binding protein. Progress report. Office of Scientific and Technical Information (OSTI), enero de 1990. http://dx.doi.org/10.2172/5701773.

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Chamovitz, Daniel A. y Zhenbiao Yang. Chemical Genetics of the COP9 Signalosome: Identification of Novel Regulators of Plant Development. United States Department of Agriculture, enero de 2011. http://dx.doi.org/10.32747/2011.7699844.bard.

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This was an exploratory one-year study to identify chemical regulators of the COP9 signalosome. Chemical Genetics uses small molecules to modify or disrupt the function of specific genes/proteins. This is in contrast to classical genetics, in which mutations disrupt the function of genes. The underlying concept is that the functions of most proteins can be altered by the binding of a chemical, which can be found by screening large libraries for compounds that specifically affect a biological, molecular or biochemical process. In addition to screens for chemicals which inhibit specific biological processes, chemical genetics can also be employed to find inhibitors of specific protein-protein interactions. Small molecules altering protein-protein interactions are valuable tools in probing protein-protein interactions. In this project, we aimed to identify chemicals that disrupt the COP9 signalosome. The CSN is an evolutionarily conserved eight-subunit protein complex whose most studied role is regulation of E3 ubiquitinligase activity. Mutants in subunits of the CSN undergo photomorphogenesis in darkness and accumulate high levels of pigments in both dark- and light-grown seedlings, and are defective in a wide range of important developmental and environmental-response pathways. Our working hypothesis was that specific molecules will interact with the CSN7 protein such that binding to its various interacting proteins will be inhibited. Such a molecule would inhibit either CSN assembly, or binding of CSN-interacting proteins, and thus specifically inhibit CSN function. We used an advanced chemical genetic screen for small-molecule-inhibitors of CSN7 protein-protein interactions. In our pilot study, following the screening of ~1200 unique compounds, we isolated four chemicals which reproducibly interfere with CSN7 binding to either CSN8 or CSN6.
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Veen, Ryan Vander, Mark Mogler, Matthew M. Erdman y D. L. Hank Harris. Preparation of GP5-M Heterodimer Glycantype Specific Recombinant Protein and Replicon Particles. Ames (Iowa): Iowa State University, enero de 2009. http://dx.doi.org/10.31274/ans_air-180814-698.

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Barkan, Alice y Zach Adam. The Role of Proteases in Regulating Gene Expression and Assembly Processes in the Chloroplast. United States Department of Agriculture, enero de 2003. http://dx.doi.org/10.32747/2003.7695852.bard.

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Chloroplasts house many biochemical processes that are essential for plant viability. Foremost, among these is photosynthesis, which requires the protein-rich thylakoid membrane system. The activation of chloroplast genes encoding thylakoid membrane proteins and the targeting and assembly of these proteins together with their nuclear-encoded partners are essential for the elaboration of the thylakoid membrane. Several nuclear-encoded proteins that regulate chloroplast gene expression and that mediate the targeting of proteins to the thylakoid membrane have been identified in recent years, and many more remain to be discovered. The abundance of such proteins is critical and is likely to be determined to a significant extent by their stability, which in turn, is influenced by chloroplast protease activities. The primary goal of this project was to link specific proteases to specific substrates, and in particular, to specific regulatory and assembly proteins. We proposed a two-pronged approach, involving genetic analysis of the consequences of the mutational loss of chloroplast proteases, and biochemical analysis of the degradation pathways of specific proteins that have been shown to control chloroplast gene expression. Our initial bioinformatic analysis of chloroplast proteases allowed us to identify the set of pro teases that is targeted to the chloroplast. We used that information to recover three Arabidopsis mutants with T - DNA insertions in specific chloroplast protease genes. We carried out the first analysis of the stability of a regulator of chloroplast gene expression (CRS2), and found that the protein is much less stable than are typical components of the photosynthetic apparatus. Genetic reagents and analytical methods were developed that have set the stage for a rapid advancement of our understanding of chloroplast proteolysis. The results obtained may be useful for manipulating the expression of transgenes in the chloroplast and for engineering plants whose photosynthetic activity is optimized under harsh environmental conditions.
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