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Au, Wing-han. "Brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TRKB) signaling in ovarian cancer". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557947.
Pełny tekst źródłaEbrahim, Seham. "Tropomyosins, N-terminal acetylation and their impact on yeast cytoskeletal function : a characterisation of novel tropomyosins from N. crassa and the N-terminal acetyltransferase, Nat3p". Thesis, Queen Mary, University of London, 2009. http://qmro.qmul.ac.uk/xmlui/handle/123456789/531.
Pełny tekst źródłaVlahovich, Nicole. "The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease". Thesis, View thesis, 2007. http://handle.uws.edu.au:8081/1959.7/32176.
Pełny tekst źródłaVlahovich, Nicole. "The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease". View thesis, 2007. http://handle.uws.edu.au:8081/1959.7/32176.
Pełny tekst źródłaA thesis presented to the University of Western Sydney, College of Health and Science, School of Natural Sciences, in fulfilment of the requirements for the degree of Doctor of Philosophy. Includes bibliographies.
歐穎嫻 i Wing-han Au. "Brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinaseB (TRKB) signaling in ovarian cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557947.
Pełny tekst źródłaRobinson, Paul John Robert. "The functional effect of disease causing mutations on thin filament regulatory proteins tropomyosin, troponin T troponin I and troponin C". Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670117.
Pełny tekst źródłaPatel, Dipesh A. Root Douglas. "Luminescence resonance energy transfer-based modeling of troponin in the presence of myosin and troponin/tropomyosin defining myosin binding target zones in the reconstituted thin filament". [Denton, Tex.] : University of North Texas, 2009. http://digital.library.unt.edu/permalink/meta-dc-9834.
Pełny tekst źródłaKotadiya, Preeyal. "Regulation Of Osteoclast Function By Alpha Gene Tropomyosins, TM-2/3 And TM-5a/5b". The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250612152.
Pełny tekst źródłaMcMichael, Brooke Kristin Trinrud. "Tropomyosin 4, myosin IIA, and myosin X enhance osteoclast function through regulation of cellular attachment structures". Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view.cgi?acc%5Fnum=osu1206052974.
Pełny tekst źródłaMcKay, Janet A. "A feasibility and exploratory study of cardiac rehabilitation in acute coronary syndrome". Thesis, University of Stirling, 2013. http://hdl.handle.net/1893/20346.
Pełny tekst źródłaMcConnell, Mark, i Mark McConnell. "Investigating the Effects of Tropomyosin D230N and cTnT R92L on the Tropomyosin Overlap Region". Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/624576.
Pełny tekst źródłaClark, Ian David. "Coupled structural responses in tropomyosin". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30625.
Pełny tekst źródłaScience, Faculty of
Chemistry, Department of
Graduate
Had, Laurence. "Tropomyosines et développement du système nerveux". Montpellier 2, 1994. http://www.theses.fr/1994MON20051.
Pełny tekst źródłaKalyva, Athanasia. "Tropomyosin heterodimers in cardiac muscle regulation". Thesis, University of Kent, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508567.
Pełny tekst źródłaBoussouf, Sabrina Eida. "Regulation of cardiac muscle contraction : effect of tropomyosin isoform expression and cardiomyopathy mutations in tropomyosin and troponin". Thesis, University of Kent, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408903.
Pełny tekst źródłaSheikh, Hajer Nisar. "Tropomyosin Phosphorylation in Cardiac Health and Disease". University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1242913472.
Pełny tekst źródłaKreuz, Andrew Joseph. "Characterization of tropomyosin mutants in Drosophila melanogaster /". The Ohio State University, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487843688958564.
Pełny tekst źródłaLendner, Matthias. "Functional analysis of tropomyosin of parasitic nematodes". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16137.
Pełny tekst źródłaParasitic worms are among the world''s most prevalent infectious diseases with more than 3.5 billion. The success of these parasites is based on their sophisticated ways to manipulate the immune system of their hosts. Interestingly, worm infections abate the risk to develop allergic disorders. How exactly parasitic worms modulate the immune system is so far largely unknown. In order to be able to investigate parasite induced modulation, this work aimed to establish RNA interference (RNAi), a method of genetic manipulation, using tropomyosin as target gene. As shown for the example of Heligmosomoides polygyrus RNAi is not or only to a small extent useful as method to genetically manipulate nematodes. This can be explained with the lack of uptake and spreading mechanisms for double stranded RNA. Furthermore, this work examined the impact of the recombinant muscle protein tropomyosin of Acanthocheilonema viteae (rAv-TMY) on the course of a rodent model of allergic airway inflammation. A four-time treatment with rAv-TMY over a period of four weeks resulted in decreased inflammatory responses in the airways. The analysis of immunological parameters showed that rAv-TMY significantly reduces the influx of inflammatory cells into the airways, especially eosinophils. The reduced eosinophil influx can be attributed to the decreased expression of IL-5, eotaxin and MCP-5 in the airways. In addition, the formation of antigen-specific IgE was impaired whereas the production of the blocking antibody IgG1 was increased. These results demonstrate the anti-allergic properties of rAv-TMY. For this reason rAv-TMY becomes an interesting model molecule for the treatment of allergic diseases. Furthermore, the comparison of allergenic, non-allergenic and modulatory tropomyosin might put some light on the nature of allergens and their molecular patterns.
Janco, Miroslav. "Characterisation of tropomyosin heterodimers carrying single cardiomyopathy mutations". Thesis, University of Kent, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.655655.
Pełny tekst źródłaLe, Sommer Caroline. "Identification de facteurs régulant en trans la maturation différentielle de la région 3' terminale de l'ARN pré-messager tropomyosine α chez Xenopus laevis". Rennes 1, 2006. http://www.theses.fr/2006REN1S009.
Pełny tekst źródłaLynn, Melissa L., i Melissa L. Lynn. "D230N-Tm Induced Dilated Cardiomyopathy and the Role of Fetal cTnT Isoform Switching in Modulating Disease Severity". Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/625579.
Pełny tekst źródłaHeydenreich, Monika. "Phänotypische Charakterisierung von Patienten mit hypertropher Kardiomyopathie und Varianten im [beta]-MHC-Gen [beta-MHC-Gen] und [alpha]-Tropomyosin-Gen [alpha-Tropomyosin-Gen]". [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=965437485.
Pełny tekst źródłaShanti, K. N. "Identification of Tropomyosin as the Major Cross-Reacting Crustacean Allergen". Thesis, Indian Institute of Science, 1994. http://hdl.handle.net/2005/103.
Pełny tekst źródłaMackenzie, Cassidy. "The properties and function of tropomyosin dimers in muscle regulation". Thesis, University of Kent, 2017. https://kar.kent.ac.uk/69463/.
Pełny tekst źródłaAsiri, Saeed Ahmed. "Effects of myopathy-causing mutations on Tropomyosin structure and function". Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/40307.
Pełny tekst źródłaPieples, Kathy. "THE FUNCTIONAL SIGNIFICANCE OF THE STRIATED ISOFORM OF TROPOMYOSIN 3 IN NORMAL AND PATHOLOGICAL STATES". University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin997992638.
Pełny tekst źródłaGraham, Ian R. "Alternative splicing of tropomyosin pre-mRNA : control in non-muscle cells". Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/35232.
Pełny tekst źródłaClayton, Joseph Emerson. "Barcoding the actin track: Differential regulation of myosin motors by tropomyosin". ScholarWorks @ UVM, 2016. http://scholarworks.uvm.edu/graddis/638.
Pełny tekst źródłaSereda, Michal Janusz. "Characterization of the molecular and immunological properties of Acanthocheilonema viteae tropomyosin". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15882.
Pełny tekst źródłaThis study describes the immunological properties of Acanthocheilonema viteae muscle-associated protein tropomyosin. A. viteae is a filarial parasite of jirds that resembles the important human parasite Onchocerca volvulus. Focus of experiments is on unraveling the functional properties of tropomyosin in the context of an infection and experimental vaccination. Additionally, allergenic potential of tropomyosin was investigated and the ability to induce high levels of specific IgE. A part of the study was also aimed at the development of anti-tropomyosin monoclonal antibodies (mAb). This study revealed that tropomyosin is a promising antigen for vaccines against filarial nematodes, however, effective only in a Th1 biased environment. Vaccination with protein or DNA resulted in 30% - 45% protection that was not associated with specific IgG or IgE. During infection tropomyosin is an allergen and leads to the production of high levels of specific IgE. Screening of synthetic peptide libraries showed 13 IgG and 11 IgE co-located epitopes and revealed cross-reactivity with other tropomyosins and sharing of IgE epitopes. mAb were raised against A. viteae tropomyosin and showed that tropomyosin is abundant on the cuticle of L3 and microfilariae of the parasite. Deglycosylation of the native protein showed that some epitopes were formed by the posttranslational modifications. Additionally, immunization shows that tropomyosin induces a similar pattern of cell activation and antibody production as aluminium hydroxide adjuvant, but leads to the induction of IL-10 and the increase of population of GR1+/CD11b+ cells. These cells are regarded as natural suppressors. Taken together, results show that A. viteae tropomyosin has immunomodulating properties and can be considered as a component of an efficient vaccine.
Clark, Ian David. "A fluorescence study of the COOH-terminus region of equine platelet tropomyosin". Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26190.
Pełny tekst źródłaScience, Faculty of
Chemistry, Department of
Graduate
Coles, J. L. "The regulation of a novel exon in the rat α-tropomyosin gene". Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597846.
Pełny tekst źródłaFairhead, Giles. "The interactions of Troponin T with Troponin C, Troponin I and Tropomyosin". Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422010.
Pełny tekst źródłaTaylor, Claire Frances. "The regulation of splicing of the human alpha sigma-tropomyosin pre-mRNA". Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/35167.
Pełny tekst źródłaPasquet, Stéphanie. "Etude de la régulation transcriptionnelle du gène alpha-tropomyosine dans les cellules musculaires". Bordeaux 2, 2003. http://www.theses.fr/2003BOR21036.
Pełny tekst źródłaWe have studied the transcriptional regulation of alpha-tropomyosin (α-TM) gene, in smooth, skeletal and cardiac muscle cells in culture. The regulatory sequences, C-rich and MCAT enhance transcription of the α-TM gene in the three muscle types. TEF-1 trans-factor plays a major role in the transcriptional regulation in the three muscle types, by binding to MCAT sequence. SRF factor seems to be involved, directly and indirectly, in the transcription activation of the gene. SRF could act indirectly in smooth and cardiac muscle cells, by enhancing TEF-1 binding, and directly in skeletal muscle cells, by binding to a CarG box. The role of TEF-1 and SRF factors could be related to their subcellular localization in smooth muscle cells
Marknell, DeWitt Åsa. "Use of recombinant allergens for component-resolved diagnostics (CRD) in IgE-mediated allergy /". Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7813.
Pełny tekst źródłaSchulz, Emily M. "To Phosphorylate or Not to Phosphorylate: The Role of Tropomyosin Phosphorylation in Cardiac Function and Disease". University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1355156757.
Pełny tekst źródłaHalsall, D. J. "The effects of troponin and tropomyosin on rabbit skeletal actomyosin subfragment 1 interactions". Thesis, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378788.
Pełny tekst źródłaGaillard, Catherine. "Le gene alpha-tropomyosine chez xenopus laevis : organisation et etude de son controle transcriptionnel". Rennes 1, 1996. http://www.theses.fr/1996REN10152.
Pełny tekst źródłaHamon, Gouault Sandra. "Etude de la maturation différentielle du gène alpha-fast tropomyosine chez xénopus Laevis : identifications d'éléments en cis régulant l'utilisation d'un exon composite interne/3' terminal". Rennes 1, 2002. http://www.theses.fr/2002REN10046.
Pełny tekst źródłaGrellscheid, S. N. "The role of cis-acting sequences in the regulation of α-tropomyosin alternative splicing". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599698.
Pełny tekst źródłaHoleman, Teryn A., i Teryn A. Holeman. "Effects of Three Cardiomyopathic-Causing Mutations (D230N, D84N, and E62Q) on the Structure and Flexibility of α-Tropomyosin". Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/624101.
Pełny tekst źródłaNadal, Magriñà Laura. "Muscarinic, adenosine and tropomyosin-related kinase B receptors modulate the neuromuscular developmental synapse elimination process". Doctoral thesis, Universitat Rovira i Virgili, 2017. http://hdl.handle.net/10803/441749.
Pełny tekst źródłaEl desarrollo del sistema nervioso periférico implica una inicial exuberante producción de neuronas y, una posterior reducción dependiente de actividad del número de sinapsis en las uniones neuromusculares (NMJ). Este proceso se denomina eliminación sináptica. Al final de la segunda semana postnatal, cada fibra muscular esta inervadas por una solo motoneurona. Los receptores muscarínicos de acetilcolina (mAChR), los receptores de adenosina (AR) y el receptor quinasa de tropomiosina B (TrkB) podrían permitir la competición entre los terminales nerviosos durante el proceso de eliminación sináptica mediante la modulación en la liberación de acetilcolina. En esta tesis se ha investigado, mediante microscopía confocal y un análisis morfológico cuantitativo, el papel de los receptores mAChRs (M1, M2 y M4), de los receptores de adenosina (A1 y A2A) y del receptor TrkB en el del proceso de eliminación en el desarrollo de la NMJ. Los resultados muestran que los receptores mAChRs, AR y el receptor TrkB promueven una desconexión axonal al inicio de la segunda semana postnatal independientemente de la maduración de los receptores de acetilcolina postsinápticos. En resumen, los receptores mAChRs, AR y el receptor TrkB retrasan el proceso de eliminación sináptica en P7 pero lo aceleran en P9. En la cooperación de estos receptores, se ha demostrado que M4 produce un efecto oclusivo sobre M1 y aditivo sobre A1 en P7. La cooperación entre M1, A1 y A2A promueve la pérdida axonal en P9, mientras que M2 es independiente de los otros receptores. M1 y TrkB cooperan para incrementar la pérdida axonal en P9 independientemente de M2 y TrkB. En conclusión, la eliminación sináptica postnatal está regulada por un mecanismo que depende de varios receptores, involucrando la cooperación de diferentes subtipos de receptores muscarínicos, de adenosina y el receptor TrkB, los cuales garantizan la monoinnervación de las sinapsis neuromusculares al final del proceso. saludable.
The development of the peripheral nervous system involves an initially exuberant production of neurons and a subsequent activity-dependent reduction in the number of synapses at the neuromuscular junctions (NMJ). This process is called synaptic elimination. At the end of the first postnatal week, each muscle fiber is innervated by a single motoneuron. Muscarinic acetylcholine receptors (mAChR), adenosine receptors (AR) and the tropomyosin-related kinase B (TrkB) receptor may allow the direct competition between nerve endings during synapse elimination through the modulation of acetylcholine release. Here, it has been investigated by confocal microscopy and quantitative morphological analysis the involvement of the individual and synergic or oclusive effect of M1-, M2- and M4-subtypes of mAChRs, A1 and A2A of ARs and TrkB in the control of the axonal elimination in developing NMJ. The results show that mAChRs, ARs and TrkB promote axonal disconnection at the beginning of the second postnatal week without affecting the postsynaptic maturation of the nicotinic receptor cluster. In summary, mAChRs, ARs and TrkB delay axonal loss at P7 but accelerate it at P9. In terms of receptor cooperation, M4 produces some occlusion of the M1 pathway and some addition to the A1 pathway at P7. The cooperation between M1, A1 and A2A receptors promotes axonal loss at P9, whereas the effect of M2 is independent of the other receptors. M1 and TrkB receptors work together to increase axonal loss rate at P9 but the effect of M2 is largely independent of the TrkB receptor. In conclusion, postnatal synapse elimination is a regulated multireceptor mechanism involving the cooperation of several muscarinic, adenosine and TrkB receptor subtypes that guarantees the monoinnervation of the neuromuscular synapses in the end of the process.
Ly, Thu, Natalia Moroz, Christopher T. Pappas, Stefanie M. Novak, Dmitri Tolkatchev, Dayton Wooldridge, Rachel M. Mayfield, Gregory Helms, Carol C. Gregorio i Alla S. Kostyukova. "The N-terminal tropomyosin- and actin-binding sites are important for leiomodin 2's function". AMER SOC CELL BIOLOGY, 2016. http://hdl.handle.net/10150/621526.
Pełny tekst źródłaBALVAY, LAURENT. "Etude de la regulation de l'epissage des exons alternatifs 6a et 6b des genes de tropomyosine". Paris 7, 1994. http://www.theses.fr/1994PA077007.
Pełny tekst źródłaHardy, Serge. "Caracterisation d'adn complementaires tropomyosines chez le xenope. Expression et modeles d'organisation des genes alpha et beta". Rennes 1, 1991. http://www.theses.fr/1991REN10014.
Pełny tekst źródłaHeydenreich, Monika. "Phänotypische Charakterisierung von Patienten mit hypertropher Kardiomyopathie und Varianten im Beta-MHC-Gen und Alpha-Tropomyosin-Gen". Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2002. http://dx.doi.org/10.18452/14777.
Pełny tekst źródłaHypertrophic Cardiomyopathy is disease of the cardiac muscle which results in an asymmetric hypertrophy especially of the interventricularseptum of the heart. It is transmitted in an autosomal dominant way. The symptoms are unspecific reaching from dyspnoe to syncopes. Sometimes the sudden death is the first manifestation of the disease. Molekular genetic researches showed that in the patients genes Mutations in proteins of the sarkomer were detectable. Two of them are alpha-Tropomyosin and beta-Myosin Heavy Chain. We examined 45 unrelated Patient of the existence of Mutations in alpha-Tropomyosin and beta-Myosin Heavy Chain. We used following Examinations: PCR, SSCP, Sequencing. A mutation in the beta-Myosin Heavy Chain were found in 6 Patients (13%), non in alpha-Tropomyosin. Generally mutations are expected in 35% in beta-Myosin Heavy Chain and 3% in alpha-Tropomyosin. Our patients seem to have mutations in genes we did not examine in this study. We detected Mutations in: Exon 13 Arg403Trp and Val411Ile, Exon 19 Arg719Trp, Exon 20 Ile736Thr, Exon 21 Leu796Phe und Exon 23 Cys905Phe. Mutation Arg 403Trp and Arg719Trp have been known in this form before, the others were new. As the phenotypes of our patients were heterogenous and not significantly to be distinguished we looked for risk factors for sudden death as described by Burn et al. 1997 within our group of patients with mutations. Five Persons showed risk factors as discribed: Exon 13 Arg403Trp and Val411Ile, Exon 19 Arg719Trp, Exon 20 Ile736Thr, Exon 21 Leu796Phe. The person with the mutation Exon 23 Cys905Phe showed no risk factors for sudden death. Our results correlate with those of earlier studies. The patient with the mutation Exon 23 Cys905Phe was classified as a low risk patient while the other mutations correlate with a further high risk.
Harder, Megan Michelle. "Morphological Changes Associated with Severe Early Onset Dilated Cardiomyopathy Caused by a Mutation in Alpha Tropomyosin". Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579427.
Pełny tekst źródłaNaye, François. "Caractérisation et rôle de TEF-1 au cours du développement embryonnaire de Xenopus Laevis". Bordeaux 2, 2007. http://www.theses.fr/2007BOR21467.
Pełny tekst źródłaCharacterization and role of TEF-1 during Xenopus laevis embryonic development. The analysis of the transcriptional control of the Xenopus laevis α-tropomyosin (α-TM) gene has led to the identification of a 30bp regulatory region. This region is conserved between all known vertebrate α-TM genes promoter ans contains an MCAT (5'-CATTCCT-3') sequence that is critical for the expression of the gene in all muscle cell types. This sequence can be bound by the transcription factor TEF-1 and is essential for a correct temporal and spatial expression of an α-TM transgene in the embryo. Studies about the role of TEF-1 in the embryonic development have been undertaken. Two genes, namely XNTEF-1, and the Xenopus Vestigial-2 gene, that encodes a TEF-1 cofactor, have been identified. The developmental expression pattern of these genes has been investigated together with their regulation by growth factors and myogenic factors. The role of TEF-1 in the developing embryo has been investigated by gain and loss of function strategies. The microinjection of high doses of either TEF-1 encoding mRNA or encoding a dominant negative protein (EnR-TEA) induced apoptosis. When low doses of TEF-1 mRNA are injected, embryos showed a ventralized phenotype. The microinjection of EnR-TEA mRNA induces the formation of a secondary dorsal axis in the embryo and blocks the neural inhibition due to BMP. In conclusion, TEF-1 could be implicated in the BMP signalling pathway which induces ventral mesoderm in the embryo
LIBRI, DOMENICO. "Caracterisation du gene codant pour l'isoforme beta de la tropomyosine chez le poulet. Etude de l'epissage alternatif". Paris 11, 1990. http://www.theses.fr/1990PA112069.
Pełny tekst źródłaZhao, Rathje Li-Sophie. "Tropomyosin in Normal and Malignant Cells and the Action of Picropodophyllin on the Microfilament and Microtubule Systems". Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-27767.
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