Добірка наукової літератури з теми "Anti–σ factor Interactions"
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Статті в журналах з теми "Anti–σ factor Interactions"
Jamithireddy, Anil Kumar, Ashish Runthala та Balasubramanian Gopal. "Evaluation of specificity determinants in Mycobacterium tuberculosis σ/anti-σ factor interactions". Biochemical and Biophysical Research Communications 521, № 4 (січень 2020): 900–906. http://dx.doi.org/10.1016/j.bbrc.2019.10.198.
Повний текст джерелаShukla, Jinal, Radhika Gupta, Krishan Gopal Thakur, Rajesh Gokhale та B. Gopal. "Structural basis for the redox sensitivity of theMycobacterium tuberculosisSigK–RskA σ–anti-σ complex". Acta Crystallographica Section D Biological Crystallography 70, № 4 (19 березня 2014): 1026–36. http://dx.doi.org/10.1107/s1399004714000121.
Повний текст джерелаAnthony, Jennifer R., Jack D. Newman та Timothy J. Donohue. "Interactions Between the Rhodobacter sphaeroides ECF Sigma Factor, σ E , and its Anti-sigma Factor, ChrR". Journal of Molecular Biology 341, № 2 (серпень 2004): 345–60. http://dx.doi.org/10.1016/j.jmb.2004.06.018.
Повний текст джерелаKwak, Min-Kyu, Han-Bong Ryu, Sung-Hyun Song, Jin-Won Lee та Sa-Ouk Kang. "Anti-σ factor YlaD regulates transcriptional activity of σ factor YlaC and sporulation via manganese-dependent redox-sensing molecular switch in Bacillus subtilis". Biochemical Journal 475, № 13 (5 липня 2018): 2127–51. http://dx.doi.org/10.1042/bcj20170911.
Повний текст джерелаCartagena, Alexis Jaramillo, Amy B. Banta, Nikhil Sathyan, Wilma Ross, Richard L. Gourse, Elizabeth A. Campbell та Seth A. Darst. "Structural basis for transcription activation by Crl through tethering of σS and RNA polymerase". Proceedings of the National Academy of Sciences 116, № 38 (4 вересня 2019): 18923–27. http://dx.doi.org/10.1073/pnas.1910827116.
Повний текст джерелаThakur, Krishan Gopal, Anagha Madhusudan Joshi та B. Gopal. "Structural and Biophysical Studies on Two Promoter Recognition Domains of the Extra-cytoplasmic Function σ Factor σC from Mycobacterium tuberculosis". Journal of Biological Chemistry 282, № 7 (4 грудня 2006): 4711–18. http://dx.doi.org/10.1074/jbc.m606283200.
Повний текст джерелаCavaliere, Paola, та Françoise Norel. "Recent advances in the characterization of Crl, the unconventional activator of the stress sigma factor σS/RpoS". Biomolecular Concepts 7, № 3 (1 червня 2016): 197–204. http://dx.doi.org/10.1515/bmc-2016-0006.
Повний текст джерелаKarlinsey, Joyce E., and Kelly T. Hughes. "Genetic Transplantation: Salmonella enterica Serovar Typhimurium as a Host To Study Sigma Factor and Anti-Sigma Factor Interactions in GeneticallyIntractable Systems." Journal of Bacteriology 188, no. 1 (January 1, 2006): 103–14. http://dx.doi.org/10.1128/jb.188.1.103-114.2006.
Повний текст джерелаTamizi, Amin-Asyraf, Norliza Abu-Bakar, Aimera-Farhana Samsuddin, Lina Rozano, Rohaiza Ahmad-Redzuan, and Abdul-Munir Abdul-Murad. "Characterisation and Mutagenesis Study of An Alternative Sigma Factor Gene (hrpL) from Erwinia mallotivora Reveal Its Central Role in Papaya Dieback Disease." Biology 9, no. 10 (October 3, 2020): 323. http://dx.doi.org/10.3390/biology9100323.
Повний текст джерелаRédly, Gyula Alan, and Keith Poole. "FpvIR Control of fpvA Ferric Pyoverdine Receptor Gene Expression in Pseudomonas aeruginosa: Demonstration of an Interaction between FpvI and FpvR and Identification of Mutations in Each Compromising This Interaction." Journal of Bacteriology 187, no. 16 (August 15, 2005): 5648–57. http://dx.doi.org/10.1128/jb.187.16.5648-5657.2005.
Повний текст джерелаДисертації з теми "Anti–σ factor Interactions"
Castro, Ana N. "The role of the anti-σ factor RsiV in stress response in Clostridium difficile and Bacillus subtilis". Thesis, University of Iowa, 2018. https://ir.uiowa.edu/etd/6069.
Повний текст джерелаEcheverry, Castano Estefania. "Novel neuroimmune interactions in the context of neuropathic pain and anti-inflammatory modulation with Transforming Growth Factor-ß1." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=117099.
Повний текст джерелаLa douleur neuropathique est un problème débilitant affectant des millions de personnes dans le monde. Cette maladie affecte la qualité de vie et apporte un fardeau économique considérable à la société. Les traitements actuels sont souvent inadéquats pour traiter ce type de douleur chronique, car ils ne procurent qu'un soulagement limité et s'accompagnent de nombreux effets secondaires indésirables et difficiles à gérer. Aussi, il est impératif que de nouveaux traitements pour la douleur neuropathique soient trouvés.Le problème de la douleur neuropathique est que la pathogenèse de cet état hypersensible est très complexe et implique des changements structuraux, psychologiques et pharmacologiques à travers l'axe neuronal (en partant du site du nerf périphérique lésé jusqu'à la moelle épinière/cerveau). Alors qu'un point de vue neurocentrique a dominé la littérature tout comme l'approche du traitement de la douleur neuropathique pendant des décennies, des travaux récents ont mis en évidence des interactions neuro-immunitaires étendues afin de caractériser la maladie. Les interactions entre les systèmes immunitaires et nerveux se produisent à différents niveaux, avec divers types de cellules immunitaires/gliales et des molécules dérivées du système immunitaire sont impliqués dans plusieurs étapes de la pathogenèse.Les quatre chapitres expérimentaux contenus dans cette thèse sont en lien avec cet état de fait récent de l'importance des mécanismes neuro-immunitaires dans la douleur neuropathique. Dans le travail présenté ici, nous avons cherché à éclaircir ces nouveaux mécanismes neuro-inflammatoires entrainant cette condition de douleur aberrante à la fois dans la moelle épinière et le nerf périphérique afin d'étudier le rôle d'une cytokine anti-inflammatoire active, TGF-β1, comme modulateur potentiel de ces mécanismes. Plusieurs mécanismes importants ont été observés: A) La modulation de la réaction inflammatoire centrale et périphérique avec TGF-β1 retarde et diminue de manière significative l'allodynie mécanique et l'hyperalgésie thermique via des actions immunosuppressives sur les cellules gliales (chapitre 2) et les macrophages (chapitre 3). Dans la moelle épinière, TGF-β1 inhibe la prolifération microgliale, l'activation des astrocytes et la libération de cytokines pro-inflammatoires et exerce des effets neuro-protecteurs entrainant une diminution de la production de MCP-1. À l'endroit de la lésion, l'exposition à TGF-β1 réduit le nombre de macrophages libérant des médiateurs inflammatoires et module différentes populations de cellule T. B) Dans le chapitre 4, nous démontrons que la douleur neuropathique induite par la lésion du nerf sciatique est associée à une augmentation de la perméabilité de la barrière hématoencéphalique (BHE). Nous avons observé que la réaction inflammatoire de la moelle déclenchée par la lésion du nerf a un rôle clé dans la modulation de la perméabilité de la BHE. Nous avons identifié MCP-1 comme étant un déclencheur endogène de la perméabilité de la BHE, cette dernière pouvant être inversée en utilisant des molécules telles que TGF-β1 et IL-10. C) La diminution sélective des microglies grâce à la MAC-1-saporine résulte en l'affaiblissement de l'hypersensibilité mécanique et thermique à la fois dans les étapes aigues et chronique suivant la lésion du nerf suggérant une contribution importante et persistante des microglies dans la pathogenèse de la douleur neuropathique. Ces résultats étendent notre compréhension des mécanismes neuro-inflammatoire de la douleur neuropathique en plus de suggérer que l'immunosuppression ou le blocage des voies de signalisation réciproques entre les cellules neurales et non-neurales offre de nouvelles opportunités à la modification de la maladie et une meilleure gestion de la douleur.
Letourneur, Didier. "Polymères fonctionnels phosphorylés : interactions biospécifiques avec des protéines humaines, anticorps anti-adn, antiphospholipides et facteurs de transcription." Paris 13, 1988. http://www.theses.fr/1988PA132010.
Повний текст джерелаJamithireddy, Anil Kumar. "Biophysical Studies on Mycobacterium Tuberculosis σ Factor – Regulatory Protein Complexes". Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4170.
Повний текст джерелаShukla, Jinal K. "Understanding the Regulatory Steps that Govern the Activation of Mycobacterium Tuberculosis σK". Thesis, 2013. http://etd.iisc.ac.in/handle/2005/3904.
Повний текст джерелаShukla, Jinal K. "Understanding the Regulatory Steps that Govern the Activation of Mycobacterium Tuberculosis σK". Thesis, 2013. http://etd.iisc.ernet.in/2005/3904.
Повний текст джерелаYunes, Sarah Ann. "The anti-cancer compound, Factor Quinolinone Inhibitor 1, inhibits stable kinetochore-microtubule attachment during mitotic progression." Thesis, 2020. https://hdl.handle.net/2144/41471.
Повний текст джерела2022-10-16T00:00:00Z
Gale, Alexander Douglas. "Interactions of viral and cellular Tumour Necrosis Factor Receptor molecules." Thesis, 2016. http://hdl.handle.net/10453/62384.
Повний текст джерелаTumour necrosis factor (TNF) is potent pro-inflammatory and anti-viral cytokine, acting via two cellular receptors, TNFR1 and TNFR2 that induces apoptosis and inflammation. Poxviruses encode homologues of TNF-receptors (viral TNFRs) that independently interact with both TNF, and simultaneously with cellular TNFRs, to subvert TNF-induced anti-viral apoptosis. The vTNFRs are expressed during poxvirus infection and are considered as bona fide virulence factors. The recently discovery of a “Pre-ligand Assembly Domain (PLAD)” within the N-terminus of the cellular TNFRs is shown to be required for receptor trimerisation and efficient cell death signalling. Whilst it has previously shown that the rabbit-trophic Myxoma (MYX) viral TNFR also contains a PLAD required for viral TNFR:cellular TNFR interactions, little is known about the human-trophic poxvirus TNFRs, nor physical characteristics of the interactions of vTNFRs and cellular TNFRs. To assess the importance of the PLAD domain in TNFR structure, function and viral subversion of TNFRs, this study focused on naturally occurring mutations in the TNFR PLAD domain, that occur in transient periodic fevers (TRAPS) – a clinical syndrome of febrile attacks of inflammation. TRAPS PLAD domain mutations were generated in a TNFR1-YFP in plasmids by site-directed mutagenesis and cloning. WT and TRAPS mutant TNFR1 constructs were transfected into U20S cells and TNFR1 location was determined by confocal microscopy. Neither WT TNFR1 nor TRAPS TNFRs were unable to be detected at the cell surface by both widefield and confocal microscopy despite published data on surface expression of WT TNFR1. WT TNFR1-YFP fusion proteins were found to be expressed within endocytic vesicles known as receptosomes and also as aggregates in a membranous structure resembling Golgi/ER. In addition it was found that TRAPS mutations in particular those affecting critical amino acids such as cysteines in disulphide bonds, display reduced TNFR-induced cell death as determined by flow cytometry. To better understand the biology of the vTNFR association with cellular TNFRs, and with WHO Smallpox committee approval, the human tropic poxviral TNFRs from Variola (Smallpox) (VAR) and Monkeypox (MPV) were synthesised and cloned as CFP/YFP and MycHis expression plasmids. Using multi-colour flow cytometry we have shown that, like the MYXT2 vTNFR, VARG4R and MPVJ2R TNFRs are potent intracellular inhibitors of TNFR1-induced cell death. As each vTNFR was able to inhibit TNFR-induced cell death, an assay was developed by flow cytometry to measure the intracellular abundance of the vTNFRs in the presence of cellular TNFR overexpression. MYXT2 was found to increase in intracellular abundance however for unknown reasons VARG4R and MPVJ2R did not convincingly increase in abundance. A structure for each of the vTNFRs was then attempted to be determined by X-ray crystallography, however bacterial expression of the both the cellular TNFRs and viral TNFRs proteins were unable to be obtained. Lastly to determine the structural orientations and conformations of cellular vTNFR interactions, a method of fluorescence resonance energy transfer (FRET) was established by flow cytometry. Using the generated C-terminal fusion -CFP and -YFP TNFRs, interactions were assessed between each of the cellular and vTNFRs. It was found that in addition to the reduced cell death TRAPS TNFRs when expressed with WT TNFR1, TRAPS mutations also cause reduced FRET possibly due to altered conformations in the receptor. Again mutations affecting more critical structural amino acids were found to have a more dramatic effect. Moreover differences were observed between mutations in distribution of FRET histograms further indicating altered network formations of higher order complexes. Next the FRET method was used to assess interactions between each of the vTNFRs with WT human TNFRs as well as with themselves and other vTNFRs. However no FRET was detectable between each of the molecules despite evidence of MYXT2 associating with human TNFR1 and TNFR2. Thus Comparative homology modelling and automated docking simulations were performed to explain possible orientations of the interactions tested in FRET. These data suggest that the interactions of vTNFRs with cellular TNFRs may possibly occur in a C-N anti-parallel orientation and not the previously predicted PLAD-PLAD interactions. Taken together, these data further our understanding of basic TNFR biology as well as for the first time characterise an entire panel of PLAD TRAPS mutations. It also furthers the characterisation of the very limited evidence of vTNFR subversion of TNFRs for the human trophic viral proteins VARG4R and MPVJ2R. Overall these results show the importance of PLAD interactions to TNFR biology and a possible new avenue in which TNFR signalling may be exploited in the development of new therapeutics.
Botha, M. E. (Mariette). "Two-hybrid analysis and attempted expression of elongation factor 1α from the cattle tick, Rhipicephalus microplus". Diss., 2013. http://hdl.handle.net/2263/31568.
Повний текст джерелаDissertation (MSc)--University of Pretoria, 2013.
Biochemistry
unrestricted
Книги з теми "Anti–σ factor Interactions"
Shengelia, Revaz. Modern Economics. Universal, Georgia, 2021. http://dx.doi.org/10.36962/rsme012021.
Повний текст джерелаЧастини книг з теми "Anti–σ factor Interactions"
Mandumpal Chacko, Sabu, and Priya Thambi Thekkekara. "Combined Effect of Metformin and Statin." In Metformin - Pharmacology and Drug Interactions. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100894.
Повний текст джерелаSethi Chopra, Dimple, Abhishek Gupta, Dhandeep Singh, and Nirmal Singh. "Anti-Inflammatory Potential of Ginseng for Wound Healing." In Ginseng - Modern Aspects of the Famed Traditional Medicine. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101167.
Повний текст джерелаТези доповідей конференцій з теми "Anti–σ factor Interactions"
McDonnell, T., C. Wincup, V. Ripoll, C. Gerveshi, A. Rahman, I. Mackie, M. Botto, and I. Giles. "PS5:99 Examining the modulatory effects of anti-serine protease antibodies upon factor xa, thrombin and complement interactions." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.144.
Повний текст джерелаWang, Changchang, Guoyu Wang, Mindi Zhang, and Qin Wu. "Wall-Pressure Fluctuations Inside Attached Cavitation." In ASME 2021 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/fedsm2021-65501.
Повний текст джерелаFulcher, C. A., R. A. Houghten, S. de Graaf Mahoney, J. R. Roberts, and T. S. Zimmerman. "SYNTHETIC PEPTIDE PROBES OF FACTOR VIII IMMUNOLOGY AND FUNCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644768.
Повний текст джерелаDevine, D. V., and W. F. Rosse. "PLATELET FACTOR H REGULATES THE ACTIVITY OF THE ALTERNATIVE PATHWAY OF COMPLEMENT ON THE SURFACE OF NORMAL AND PAROXYSMAL NOCTURNAL HEMOGLOBINURIA PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643979.
Повний текст джерелаGewirtz, A., W. Y. Xu, B. Rucinski, and S. Niewiarowski. "SELECTIVE INHIBITION OF HUMAN MEGAKARYOCYTOPOIESIS IN VITRO BY HIGHLY PURIFIED PLATELET FACTOR 4." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644621.
Повний текст джерелаCroccolo, Dario, Massimiliano De Agostinis, Stefano Fini, Giorgio Olmi, Francesco Robusto, Omar Cavalli, and Nicolò Vincenzi. "The Influence of Material, Hardness, Roughness and Surface Treatment on the Frictional Characteristics of the Underhead Contact in Socket-Head Screws." In ASME 2018 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/pvp2018-84530.
Повний текст джерелаSchmid, Peter, and Emmanuel de Langre. "Transient Growth Before Coupled-Mode Flutter." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32200.
Повний текст джерелаNachman, R. L., R. L. Silverstein, and A. S. Asch. "THROMBOSPONDIN: CELL BIOLOGY OF AN ADHESIVE GLYCOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644653.
Повний текст джерелаMarquerie, G., A. Duperray, G. Uzan, and R. Berthier. "BIOSYNTHETIC PATHWAYS OF THE PLATELET FIBRINOGEN RECEPTOR IN HUMAN MEGAKARYOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642954.
Повний текст джерелаЗвіти організацій з теми "Anti–σ factor Interactions"
Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.
Повний текст джерелаCitovsky, Vitaly, and Yedidya Gafni. Viral and Host Cell Determinants of Nuclear Import and Export of the Tomato Yellow Leaf Curl Virus in Tomato Plants. United States Department of Agriculture, August 2002. http://dx.doi.org/10.32747/2002.7585200.bard.
Повний текст джерелаAltstein, Miriam, and Ronald J. Nachman. Rational Design of Insect Control Agent Prototypes Based on Pyrokinin/PBAN Neuropeptide Antagonists. United States Department of Agriculture, August 2013. http://dx.doi.org/10.32747/2013.7593398.bard.
Повний текст джерела