Teses / dissertações sobre o tema "Molecular adhesion"
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Townsend, Paul Andrew. "The molecular basis of osteoblast adhesion". Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263651.
Texto completo da fonteLougheed, Caroline. "Targeting focal adhesion signaling in cancer and acquired resistance to focal adhesion kinase inhibitors". Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=94996.
Texto completo da fonteDans la progression du cancer, le développement de métastases est caractéristique de la phase terminale et rend le traitement difficile. Afin que des métastases se dévelopment, les cellules cancéreuses doivent acquérir de la motilité ainsi qu'un phénotype invasif. Considéré come l'une des plus importantes protéines participant dans la motilité cellulaire, la prot éine Focal Adhesion Kinase (FAK) a émergé comme une bonne cible thérapeutique pour l'inhibition de métastases par la création de drogues ciblées et de petites molécules inhibitrices. Par conséquent, une molécule inhibitrice de l'activation de FAK et sa signalisation a été récemment développée. Cependant, J'ai demontré que la résistance est commune parmis ces drogues. Le dévelopement et la classification des clones de cellules résistantes ont permi d'élucider un mécanisme impiquant en partie une amplification de l'activité FAK; ce mécanisme permetter a de découvrir des analogues de deuxième génération pour surmonter ou éviter la résistance. L'ensemble de données présentées ci-dessous supportet le rôle de FAK comme une cible importante dans la prévention de métastases et exposent les futur directions pour contourner la résistance aux inhibiteurs de FAK.
Harrison, O. J. "The molecular mechanism of cadherin-mediated adhesion". Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603783.
Texto completo da fonteMinett, William T. "Cell adhesion on synthetic polymer substrates". Thesis, Aston University, 1986. http://publications.aston.ac.uk/14512/.
Texto completo da fonteCho, Jae Youl. "Molecular mechanism of CD98 function". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249677.
Texto completo da fonteWu, Tao. "Structure-function analysis of vascular tethering molecules using atomic force microscope". Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/31844.
Texto completo da fonteCommittee Chair: Zhu, Cheng; Committee Member: Barry, Bridgette; Committee Member: Boyan, Barbara; Committee Member: McEver, Rodger; Committee Member: McIntire, Larry. Part of the SMARTech Electronic Thesis and Dissertation Collection.
Eriksson, Malin. "The Influence of Molecular Adhesion on Paper Strength". Doctoral thesis, Stockholm, Department of Fibre and Polymer Technology, School of Chemical Science and Engineering, KTH, Royal Institute of Technlology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-4101.
Texto completo da fonteBuehler, Betul. "Molecular Adhesion and Friction at Elastomer/Polymer Interfaces". University of Akron / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=akron1164649632.
Texto completo da fonteKillock, David James. "Molecular characterisation of L-selectin-dependent adhesion and signalling". Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.512055.
Texto completo da fonteGideonsson, Pär. "Helicobacter pylori : molecular insights into regulation of adhesion properties". Doctoral thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-120466.
Texto completo da fontePiper, James Wilson. "Force dependence of cell bound E-selectin/carbohydrate ligand binding characteristics". Diss., Georgia Institute of Technology, 1997. http://hdl.handle.net/1853/18388.
Texto completo da fonteSjöström, Annika E. "Pathogenecity-associated genes modulate Escherichia coli adhesion and motility". Doctoral thesis, Umeå universitet, Molekylärbiologi (Medicinska fakulteten), 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-22302.
Texto completo da fonteAfar, Daniel E. H. "Phosphorylation and cell adhesion properties of myelin-associated glycoprotein isoforms". Thesis, University of Ottawa (Canada), 1992. http://hdl.handle.net/10393/7517.
Texto completo da fonteLeung, Yu Hing Nelly. "Carcinoembryonic antigen cell adhesion molecule 1: cancer and metabolic regulation". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18740.
Texto completo da fonteLa glycoprotéine CEACAM1 (Carcinoembryonic antigen cell adhesion molecule 1) est une molécule d'adhésion appartenant à la famille des CEA (Antigène carcinoembryonnaire). CEACAM1 se retrouve à la surface des cellules épithéliales, endothéliales, et hématopoétiques, du tube digestif, des organes reproducteurs, du foie, des poumons et des reins. CEACAM1 présente plusieurs fonctions: inhibition de la réponse immunitaire, adhésion cellulaire, clairance de l'insuline, apoptose et prolifération cellulaire, angiogénèse, et rôle de suppresseur de tumeurs. L'expression de CEACAM1 est souvent diminuée dans plusieurs cas de cancers humains dont le côlon, le foie, la prostate, et 30% des cancers du sein. Le modèle de souris Ceacam1-/- a été utilisé afin d'étudier le rôle de CEACAM1 dans la formation de tumeur. En l'absence de CEACAM1, le tissu épithélial de l'intestin grêle et du côlon subit moins d'apoptose. En contrepartie, une augmentation de la prolifération est détectée dans le côlon des souris Ceacam1-/-. L'absence de CEACAM1 n'étant pas suffisante pour induire l'apparition de tumeurs, nous avons utilisé un cancérogène chimique, l'azoxymethane. Les tumeurs observées dans le côlon des souris Ceacam1-/- s'avèrent être plus importantes que celles des souris contrôles. Le désavantage de l'utilisation de l'azoxymethane est que celui-ci provoque des mutations dans plusieurs gènes plus ou moins définis. Afin de comprendre la contribution de CEACAM1 dans le développement tumoral, la souris Ceacam1-/- a été croisée avec la souris Apc1638N/+ qui forme spontanément des tumeurs dans l'intestin grêle. Les souris Apc1638N/+: Ceacam1-/- développent plus de tumeurs présentant un phénotype tumoral plus agressif que celui formé dans les souris Apc1638N/+. Par ailleurs, les cellules épithéliales de l'intestin grêle Ceacam1-/- montrent une dérégulation de la voie de signalisation Wnt. CEACAM1 étant un facteu
Gandhi, Neha Sureshchandra. "Molecular modelling of platelet endothelial cell adhesion molecule 1 and its interaction with glycosaminoglycans". Thesis, Curtin University, 2007. http://hdl.handle.net/20.500.11937/1513.
Texto completo da fonteMcNulty, Clare A. "Studies on the molecular basis of eosinophil adhesion to endothelium". Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29391.
Texto completo da fonteWright, Ann Heather. "The molecular basis of leukocyte adhesion deficiency in six patients". Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239257.
Texto completo da fonteCooper, Sharon Rose. "δ-Protocadherin Function: From Molecular Adhesion Properties to Brain Circuitry". The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492457066344753.
Texto completo da fonteChen, Wei. "Molecular dynamics simulations of binding, unfolding, and global conformational changes of signaling and adhesion molecules". Diss., Atlanta, Ga. : Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/28118.
Texto completo da fonteCommittee Chair: Zhu, Cheng; Committee Member: Harvey, Stephen; Committee Member: Hud, Nicholas; Committee Member: Zamir, Evan; Committee Member: Zhu, Ting.
Källström, Helena. "Molecular and cellular mechanisms during adherence and cell signaling of pathogenic Neisseria to host cells /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3848-2/.
Texto completo da fonteZhou, Hua 1963. "Molecular mechanisms of intercellular adhesion mediated by carcinoembryonic antigen family members". Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41172.
Texto completo da fonteNicholson, Martin William Michael. "Molecular analysis of the leukocyte cell-surface adhesion protein L-selectin". Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260752.
Texto completo da fonteShirure, Venktesh S. "Molecular Mechanisms of Circulating Tumor Cell Adhesion in Breast Cancer Metastasis". Ohio University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1357706517.
Texto completo da fontePerera, Hettiarachchige Dhanuja Deepamalee. "Molecular Basis of the Role of Kindlin 2 in Cell Adhesion". Cleveland State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=csu1295461683.
Texto completo da fonteCarulli, Sonia. "Molecular basis of syndecan-1 mediated cell adhesion to laminin 332". Thesis, Lyon 1, 2011. http://www.theses.fr/2011LYO10134.
Texto completo da fonteThe HSPG receptor syndecan-1 interacts with the carboxy-terminal LG4/5 domain in laminin 332 to participate in keratinocyte migration by inducing formation of cytoskeleton related protrusive structures. We have shown that syndecan-1 mediated cell adhesion occurs in heparan sulphate and chondroitin sulphate dependent manner and that these two glycosaminoglycan (GAG) chains bind independently to LG4/5 with different affinities. To identify residues involved in the interaction of the LG4/5 domain with syndecan-1 and to apprehend the molecular basis of the GAGs interaction specificity, we have used a site-directed mutagenesis approach of the recombinant LG4/5 fragment. The residues identified as conserved heparin binding residues throughout laminins, as well as “candidate” basic residues identified through predictive approaches, have been replaced by the neutral residue glutamine. All LG4/5 proteins carrying a hexa-histidine tag at their C-terminal end were expressed in mammalian cells. The produced proteins were purified and characterized biochemically. Circular dichroism studies performed on all mutagenised proteins showed that the overall structure of each mutant is comparable to that of the wild type protein. Heparin affinity chromatography analysis allowed us to identify a major heparin binding site in the LG4/5 domain surrounded by several minor GAG binding sites. Surface plasmon resonance analysis of mutated LG4/5 proteins-heparan sulphate interaction confirmed these results. These findings were well correlated with our in cellulo syndecan-1 mediated cell adhesion as the lack of this major heparin binding site totally abrogated cell adhesion. Pull down experiments allowed us to show that this heparin binding site sequence is responsible not only for the interaction of the receptors syndecan-1 but also for syndecan-4 suggesting that additional cellular functions may be carried by this sequence. Our structural predictions suggest that the LG4/5 in laminin 332 encompasses a major GAG binding site surrounded by a track of converging positively charged residues
Hur, Sunyoung. "Molecular mechanism of barnacle adhesion : a structural approach and underlying biochemistry". Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS572.pdf.
Texto completo da fonteBarnacles adhere themselves robustly and permanently to diverse underwater substrates through strong interactions of a multi-protein complex layer called the “cement”. However, the intermolecular interactions responsible for the strong adhesive properties of the barnacle cement remains poorly understood. A central hypothesis of this thesis is that underwater properties of the cement complex are intimately linked to the molecular characteristics of cement proteins (CPs) forming the cement complex. Previous studies have shown that the cement is made of amyloid-like nanofibrils that may contribute to adhesion. However, the protein responsible for the formation of these nanofibrils remain unknown. In this study, the nanoscale morphological features of recombinant cement proteins (CPs) from the barnacle Megabalanus rosa (MrCP19 and MrCP20, with the numbers indicating molecular weight of 19 kDa and 20 kDa respectively) were characterized by Circular Dichroism (CD) measurement, Thioflavin T (ThT) assay, Atomic Force Microscopy (AFM), and Transmission Electron Microscopy (TEM), suggesting the potential to form nano-fibrillar structures under certain conditions. Based on the proteins’ primary structure and surface morphology, mechanical, biochemical, and antimicrobial studies were conducted to understand the unique roles of these interfacial proteins on barnacle growth and surface attachment process, for instance biomineralization and biodegradation control. Measurements using Surface Force Apparatus (SFA) and Quartz Crystal Microbalance with Dissipation monitoring (QCM-D) illustrated that electrostatic interactions play a key role in surface adsorption and adhesion of MrCP19 and MrCP20. In addition, the mutual influence of barnacle base plate growth (calcium carbonate mineralization) and the adjacent cement protein MrCP20 fibrillation was investigated using self-assembled monolayer (SAM) functionalized gold surfaces, Raman spectroscopy, QCM-D, X-ray photoelectron spectrometer (XPS), and Attenuated total reflectance Fourier transform infrared spectroscopy (ATR-FTIR). Concurrently, the influence of the external substrate adjacent cement protein MrCP19 on bacteria cells which are present in biofilm on underwater surfaces in marine environment was demonstrated using different microbiology tests including zone of inhibition test, Minimum inhibitory concentration (MIC) assay, TEM, fluorescence study, and so on. More interestingly, an intriguing hypothesis regarding amyloid fibrillation process and antimicrobial activity was suggested. Based on these preliminary examinations, the two interfacial CPs showed distinctive potential responsibilities on barnacle settlement not only with its adhesion but also with other functional roles at the interfaces. This work will improve our knowledge about individual contributions of MrCP19 and MrCP20 in cement complex and hence in overall underwater adhesion capacity of barnacles. In this regard, the thesis aims at providing molecular guidelines towards the development of CPs inspired polymeric (peptide or protein based) mimics from this bio-adhesive molecular system
Loumrhari, Fatine. "Investigation of Rab GTPase interaction with focal adhesion proteins in breast cancer cells". Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86771.
Texto completo da fonteLe cancer invasif du sein reste une maladie extrêmement courante et une cause majeure de mortalité parmi les personnes atteintes du cancer. Un événement par lequel les cellules du cancer se propagent est initié par l'acquisition de propriétés mobiles conduites par le remodellement du cytosquelette cellulaire et par le roulement dynamique de protéines d'adhérence focale (FA); relient la matrice extracellulaire au cytosquelette cellulaire. Le cancer invasif du sein a été associé avec l'expression élevée de certaines proteines surnommées les Rab GTPases. Ils sont connus comme des regulateurs essentiels dans la circulation membraneuse y compris le recyclage des recepteurs incluant celles des integrins, protéines d'adhérence focale qui agissent en tant que mediateur pour l'adherence des cellules a la matrice extracellulaire. Leur expression élevée, a en fait, favorisé la migration et l'invasion des cellules, contribuable a la métastase du cancer. Auparavant, des études "proteomiques" sur des cellules non-invasives contre des cellules invasives du cancer du sein ont révélé un roulement rapide de protéines d'adhérence focales (FA) dans les cellules invasives, ainsi q'une expression différentielle de plusieurs membres de Rab GTPases, y compris Rab5, Rab11 et Rab7. Ainsi, nous testons l'hypothèse que Rab GTPase interagit avec la protein kinase d'adhérence focale (FAK), qui sert comme mediateur pour les voies de transduction des signaux aux sites d'adherence focale. Nous supposons aussi que les Rabs pourraient jouer un role important dans la regulations de la circulation de FA dans le cancer invasive du sein. Les experiences faites avec l'immunofluorecence et l'immunoprecipitation révèlent que Rab11 et FAK interagissent et colocalisent ensembles. Le développement de lignes de cellules où les Rabs ont été diminués en utilisent le siRNA démontre son effet sur la migration de cellules. Je propose que Rab11 est un élément decisif qui po
McCuaig, Kimberly. "Alternative splicing and adhesion properties of a mouse carcinoembryonic antigen gene family member". Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56679.
Texto completo da fonteEfstathiou, Jason Alexander. "The role of adhesion molecules in colorectal carcinogenesis". Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670210.
Texto completo da fonteGann, Reed N. "Host Signaling Response to Adhesion of Bifidobacterium infantis". DigitalCommons@USU, 2010. https://digitalcommons.usu.edu/etd/586.
Texto completo da fonteTsen, Guoshan. "Molecular characterization of a heparan sulfate proteoglycan that interacts with the neural cell adhesion molecule (NCAM) /". The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487945320760721.
Texto completo da fonteThwaites, Tristan. "Characterisation of the molecular basis underlying Chlamydial subversion of focal adhesion signaling". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/40508.
Texto completo da fonteBuckley, Christopher Dominic. "Molecular analysis of IgSF-integrin interactions : their role in leukocyte endothelial adhesion". Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320117.
Texto completo da fonteQouta, Lolita Abdulla. "The biochemistry and molecular biology of intercellular adhesion in plant tissue culture". Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/302/.
Texto completo da fonteNewe, Abigail Lucy. "Unearthing the molecular mechanisms that govern L-selectin-dependent adhesion and migration". Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/unearthing-the-molecular-mechanisms-that-govern-lselectindependent-adhesion-and-migration(8f22370e-34b7-447f-98c2-dd1713036a84).html.
Texto completo da fonteStrömberg, Nicklas. "Studies on receptor glycosphingolipids for bacterial adhesion molecular details as revealed by a novel solid phase assay /". Göteborg : Dept. of Medical Biochemistry and Faculty of odontology, University of Göteborg, 1988. http://books.google.com/books?id=gslpAAAAMAAJ.
Texto completo da fonteChong, William Woei Fong. "Adhesive and molecular friction in tribological conjunctions". Thesis, Cranfield University, 2012. http://dspace.lib.cranfield.ac.uk/handle/1826/7160.
Texto completo da fonteLiu, Qingde. "Molecular and physical determinants of fibrinogen-dependent platelet aggregation and adhesion in flow". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ50213.pdf.
Texto completo da fonteBohil, Aparna Bhaskar Cheney Richard E. "Myosin-X is a molecular motor central to filopodia formation, adhesion, and signaling". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,713.
Texto completo da fonteTitle from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Cell and Molecular Physiology - School of Medicine." Discipline: Cell and Molecular Physiology; Department/School: Medicine.
Liu, Qingde 1963. "Molecular and physical determinants of fibrinogen-dependent platelet aggregation and adhesion in flow". Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35909.
Texto completo da fonteThough resting platelets are able to adhere to surface-bound Fg, this adhesion efficiency is much lower than that of the adhesion of the activated platelets. The adhesion efficiency of both resting and activated platelets to surface-adsorbed Fg decreases with increasing shear rate from 100 s -1 to 2,000 s-1. However, the decrease of the adhesion efficiency of the resting platelets is more marked than the decrease of the adhesion efficiency of the activated ones. Thus, the higher the shear rates, the larger the difference in the adhesion efficiencies between resting and activated platelets. However, due to the higher collision frequencies at higher shear rates, the adhesion of resting platelets was maintained at a similar level from shear rates of 300--2,000 s-1, while the adhesion of activated platelets kept increasing from 100 s -1 to 2,000 s-1. These data indicate that platelet activation is an efficient regulation pathway for platelet adhesion to surfaces.
Thekke, Palasseri Vipin Madhavan. "Molecular Mechanisms Underlying Adhesion and Regulation of Virulence of Human Enterotoxigenic Escherichia coli". Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367416.
Texto completo da fonteThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Director, Laura Taylor. "A Novel Approach For The Identification of Cytoskeletal and Adhesion A-Kinase Anchoring Proteins". ScholarWorks @ UVM, 2014. http://scholarworks.uvm.edu/graddis/264.
Texto completo da fonteCrabb, Edward B. "An Evaluation of Induced Shear Stress on Endothelial Cellular Adhesion Molecules". VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5911.
Texto completo da fonteIsmail, Hodan. "Vascular endothelial growth factor and angiopoietin-1 regulate leukocyte adhesion to endothelial cells through the nuclear receptor Nur77". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107844.
Texto completo da fonteLes facteurs de croissance endothélials vasculaires (VEGF) et l'angiopoïétine 1 (Ang-1) sont de régulateurs essentiels de l'angiogénèse. En outre, tous les deux ont été découverts pour leur participation dans le processus d'inflammation: VEGF comme pro-infammatoire et Ang-1 comme médiateur anti-inflammatoire. Nur77 est un membre de la famille des récepteurs orphelins (NR4A) qui comprend Nurr1 and Nor1 et jouent un rôle dans la régulation de l'inflammation vasculaire; toutefois cela n'est pas encore totalement compris. Le but de cette étude était d'évaluer si l'expression de Nur77 dans les cellules endothéliales (ECs) sert de mécanisme de rétroaction négatif conçu pour inhiber l'induction de NFκB en réduisant l'expression de la E-selectin et de VCAM1 induite par VEGF, ainsi que l'adhésion des leucocytes aux ECs, et pour agir en médiateur de la suppression de l'activation des ECs induite par le traitement avec Ang-1. Le traitement des cellules endothéliales humaines de la veine ombilicale (HUVECs) soit avec VEGF ou Ang-1 induit de façon significative et transitoire l'expression de Nur77 et augmente la Phosphorylation de HDAC7 PKD dépendante et la mobilisation du noyau vers le cytosol. Les HUVECs transduits avec les adénovirus exprimant HDAC7 muté ou un dominant négatif PKD1 inhibent VEGF, mais pas l'expression de Nur77 induit par Ang-1. L'inhibition de la PI3K et de ERK1/2 aboutit à la suppression de l'expression de Nur77 induit par Ang-1 alors que l'inhibition de JNK résulte de façon significative en une plus grande induction de Nur77 par Ang-1. L'essai d'activité de liaison de NFκB ainsi que celui du gel de retardation révèlent que Nur77 inhibe l'activité de NFκB induit par VEGF. La surexpression de Nur77 a montré une sur-régulation dépendante de la titration de l'ARNm et de l'expression protéique de IκBα, pas évidente avec les HUVECs transduites avec les virus exprimant la forme dominante négative de Nur77 (Ad-dnNur77). J'ai trouvé que Nur77 réprimait l'ARNm et l'expression protéique de E-selectin and VCAM1 induit par VEGF. De façon importante, le rôle de Nur77 dans l'adhésion des leucocytes aux ECs induits par les cytokines a été examiné. L'adhérence des cellules U937 aux HUVECs activées par VEGF était réprimée par la surexpression de Nur77 alors que la perte de Nur77 par l'ARNsi d'interférence résulte dans une augmentation de l'adhésion. De manière intéressante, Ang-1 était capable d'amortir l'adhésion aux monocouches de HUVECs induite par VEGF. Je conclus que Nur77 joue un rôle important en fournissant un mécanisme de rétroaction négatif conçu pour atténuer la réponse pro-infammatoire induite par VEGF à travers l'inhibition sélective de l'activation de NFκB. Par ailleurs Nur77 en partie, peut être vital pour les réponses anti-inflammatoires d'Ang-1.
Turaga, Soumya. "TUMOR CELL INTRINSIC AND EXTRINSIC FUNCTIONS OF JUNCTIONAL ADHESION MOLECULE-A (JAM-A) IN GLIOBLASTOMA". Cleveland State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=csu1575548662111326.
Texto completo da fonteDos, Santos Washington Luis Conrado. "Molecular characteristics of the endothelial cell surface : role in the control of lymphology adhesion". Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283196.
Texto completo da fonteCopeman, Kayla. "Evaluating Epoxy Cure And Adhesion Strength Through Single-Sided Nmr Measurements Of Molecular Mobility". W&M ScholarWorks, 2021. https://scholarworks.wm.edu/etd/1627047854.
Texto completo da fonteCheng, Ling. "MOLECULAR MECHANISM OF L1CAM FUNCTION: AXON GROWTH AND GUIDANCE". Connect to online version, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1081281361.
Texto completo da fonteKambe, Yusuke. "Molecular Design of Silk Fibroin for Functional Scaffolds". 京都大学 (Kyoto University), 2013. http://hdl.handle.net/2433/174922.
Texto completo da fonteVan, Order Jon P. "Molecular modeling of intermediate order in polymer glasses". Diss., Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/10134.
Texto completo da fonte