Bibliografías temáticas / Utrophin

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Literatura académica sobre el tema "Utrophin"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 1 de febrero de 2022

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Artículos de revistas sobre el tema "Utrophin"

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Marshall, Jamie L., Johan Holmberg, Eric Chou, Amber C. Ocampo, Jennifer Oh, Joy Lee, Angela K. Peter, Paul T. Martin, and Rachelle H. Crosbie-Watson. "Sarcospan-dependent Akt activation is required for utrophin expression and muscle regeneration." Journal of Cell Biology 197, no. 7 (June 25, 2012): 1009–27. http://dx.doi.org/10.1083/jcb.201110032.

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Utrophin is normally confined to the neuromuscular junction (NMJ) in adult muscle and partially compensates for the loss of dystrophin in mdx mice. We show that Akt signaling and utrophin levels were diminished in sarcospan (SSPN)-deficient muscle. By creating several transgenic and knockout mice, we demonstrate that SSPN regulates Akt signaling to control utrophin expression. SSPN determined α-dystroglycan (α-DG) glycosylation by affecting levels of the NMJ-specific glycosyltransferase Galgt2. After cardiotoxin (CTX) injury, regenerating myofibers express utrophin and Galgt2-modified α-DG aro
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2

Perkins, Kelly J., Utpal Basu, Murat T. Budak, Caroline Ketterer, Santhosh M. Baby, Olga Lozynska, John A. Lunde, Bernard J. Jasmin, Neal A. Rubinstein, and Tejvir S. Khurana. "Ets-2 Repressor Factor Silences Extrasynaptic Utrophin by N-Box–mediated Repression in Skeletal Muscle." Molecular Biology of the Cell 18, no. 8 (August 2007): 2864–72. http://dx.doi.org/10.1091/mbc.e06-12-1069.

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Utrophin is the autosomal homologue of dystrophin, the protein product of the Duchenne's muscular dystrophy (DMD) locus. Utrophin expression is temporally and spatially regulated being developmentally down-regulated perinatally and enriched at neuromuscular junctions (NMJs) in adult muscle. Synaptic localization of utrophin occurs in part by heregulin-mediated extracellular signal-regulated kinase (ERK)-phosphorylation, leading to binding of GABPα/β to the N-box/EBS and activation of the major utrophin promoter-A expressed in myofibers. However, molecular mechanisms contributing to concurrent
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Moorwood, Catherine, Neha Soni, Gopal Patel, Steve D. Wilton, and Tejvir S. Khurana. "A Cell-Based High-Throughput Screening Assay for Posttranscriptional Utrophin Upregulation." Journal of Biomolecular Screening 18, no. 4 (October 30, 2012): 400–406. http://dx.doi.org/10.1177/1087057112465648.

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Duchenne muscular dystrophy (DMD) is a devastating muscle-wasting disease caused by mutations in the dystrophin gene. Utrophin is a homologue of dystrophin that can compensate for its absence when overexpressed in DMD animal models. Utrophin upregulation is therefore a promising therapeutic approach for DMD. Utrophin is regulated at both transcriptional and posttranscriptional levels. Transcriptional regulation has been studied extensively, and assays have been described for the identification of utrophin promoter-targeting molecules. However, despite the profound impact that posttranscription
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4

Fabbrizio, E., J. Latouche, F. Rivier, G. Hugon, and D. Mornet. "Re-evaluation of the distributions of dystrophin and utrophin in sciatic nerve." Biochemical Journal 312, no. 1 (November 15, 1995): 309–14. http://dx.doi.org/10.1042/bj3120309.

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Differential expression of proteins belonging to the dystrophin family was analysed in peripheral nerves. In agreement with previous reports, no full-size dystrophin was detectable, only Dp116, one of the short dystrophin products of the Duchenne muscular dystrophy (DMD) gene. We used specific monoclonal antibodies to fully investigate the presence of utrophin, a dystrophin homologue encoded by a gene located on chromosome 6q24. Evidence is presented here of the presence of two potential isoforms of full-length utrophin in different nerve structures, which may differ by alternative splicing of
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5

Khurana, Tejvir S., Alan G. Rosmarin, Jing Shang, Thomas O. B. Krag, Saumya Das та Steen Gammeltoft. "Activation of Utrophin Promoter by Heregulin via theets-related Transcription Factor Complex GA-binding Protein α/β". Molecular Biology of the Cell 10, № 6 (червень 1999): 2075–86. http://dx.doi.org/10.1091/mbc.10.6.2075.

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Utrophin/dystrophin-related protein is the autosomal homologue of the chromosome X-encoded dystrophin protein. In adult skeletal muscle, utrophin is highly enriched at the neuromuscular junction. However, the molecular mechanisms underlying regulation of utrophin gene expression are yet to be defined. Here we demonstrate that the growth factor heregulin increases de novo utrophin transcription in muscle cell cultures. Using mutant reporter constructs of the utrophin promoter, we define the N-box region of the promoter as critical for heregulin-mediated activation. Using this region of the utro
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MORRIS, Glenn E., Nguyen thi MAN, Nguyen thi Ngoc HUYEN, Alexander PEREBOEV, John KENDRICK-JONES, and Steven J. WINDER. "Disruption of the utrophin–actin interaction by monoclonal antibodies and prediction of an actin-binding surface of utrophin." Biochemical Journal 337, no. 1 (December 17, 1998): 119–23. http://dx.doi.org/10.1042/bj3370119.

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Monoclonal antibody (mAb) binding sites in the N-terminal actin-binding domain of utrophin have been identified using phage-displayed peptide libraries, and the mAbs have been used to probe functional regions of utrophin involved in actin binding. mAbs were characterized for their ability to interact with the utrophin actin-binding domain and to affect actin binding to utrophin in sedimentation assays. One of these antibodies was able to inhibit utrophin–F-actin binding and was shown to recognize a predicted helical region at residues 13–22 of utrophin, close to a previously predicted actin-bi
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James, M., A. Nuttall, J. L. Ilsley, K. Ottersbach, J. M. Tinsley, M. Sudol, and S. J. Winder. "Adhesion-dependent tyrosine phosphorylation of (beta)-dystroglycan regulates its interaction with utrophin." Journal of Cell Science 113, no. 10 (May 15, 2000): 1717–26. http://dx.doi.org/10.1242/jcs.113.10.1717.

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Many cell adhesion-dependent processes are regulated by tyrosine phosphorylation. In order to investigate the role of tyrosine phosphorylation of the utrophin-dystroglycan complex we treated suspended or adherent cultures of HeLa cells with peroxyvanadate and immunoprecipitated (beta)-dystroglycan and utrophin from cell extracts. Western blotting of (β)-dystroglycan and utrophin revealed adhesion- and peroxyvanadate-dependent mobility shifts which were recognised by anti-phospho-tyrosine antibodies. Using maltose binding protein fusion constructs to the carboxy-terminal domains of utrophin we
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Winder, S. J., L. Hemmings, S. K. Maciver, S. J. Bolton, J. M. Tinsley, K. E. Davies, D. R. Critchley, and J. Kendrick-Jones. "Utrophin actin binding domain: analysis of actin binding and cellular targeting." Journal of Cell Science 108, no. 1 (January 1, 1995): 63–71. http://dx.doi.org/10.1242/jcs.108.1.63.

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Utrophin, or dystrophin-related protein, is an autosomal homologue of dystrophin. The protein is apparently ubiquitously expressed and in muscle tissues the expression is developmentally regulated. Since utrophin has a similar domain structure to dystrophin it has been suggested that it could substitute for dystrophin in dystrophic muscle. Like dystrophin, utrophin has been shown to be associated with a membrane-bound glycoprotein complex. Here we demonstrate that expressed regions of the predicted actin binding domain in the NH2 terminus of utrophin are able to bind to F-actin in vitro, but d
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9

Dubowitz, Victor. "Utrophin euphoria." Neuromuscular Disorders 7, no. 1 (January 1997): 5–6. http://dx.doi.org/10.1016/s0960-8966(96)00432-4.

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Gramolini, Anthony O., Guy Bélanger, and Bernard J. Jasmin. "Distinct regions in the 3′ untranslated region are responsible for targeting and stabilizing utrophin transcripts in skeletal muscle cells." Journal of Cell Biology 154, no. 6 (September 10, 2001): 1173–84. http://dx.doi.org/10.1083/jcb.200101108.

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In this study, we have sought to determine whether utrophin transcripts are targeted to a distinct subcellular compartment in skeletal muscle cells, and have examined the role of the 3′ untranslated region (UTR) in regulating the stability and localization of utrophin transcripts. Our results show that utrophin transcripts associate preferentially with cytoskeleton-bound polysomes via actin microfilaments. Because this association is not evident in myoblasts, our findings also indicate that the localization of utrophin transcripts with cytoskeleton-bound polysomes is under developmental influe
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Tesis sobre el tema "Utrophin"

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Broderick, Michael James Francis. "The utrophin-actin interface." Thesis, University of Glasgow, 2005. http://theses.gla.ac.uk/30889/.

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The spectrin superfamily is a diverse group of proteins variously involved in cross- linking, bundling and binding to the F-actin cytoskeleton. These proteins are modular in nature and interaction with actin occurs, at least in part, via CH domain containing ABDs. The actin binding domains of the spectrin superfamily proteins are all very similar in overall structure however the functions of the individual proteins differ greatly. Utrophin is a member of the spectrin superfamily and has been used extensively to investigate and model the association of actin-binding domains with F- actin; howev
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2

Dennis, Carina Louise. "Promoter studies of the utrophin gene." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320271.

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Pearce, Marcela. "Genomic structure of the human utrophin gene." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318897.

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Fisher, Rosie. "Utrophin in therapy of Duchenne muscular distrophy." Thesis, University of Oxford, 2001. http://ora.ox.ac.uk/objects/uuid:192fbccd-d037-4ce8-b1cd-0315afe1860d.

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James, Marian. "Monoclonal antibody studies of dystrophin and utrophin." Thesis, University of Salford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360455.

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Moores, Carolyn Ann. "Structure-function analysis of the utrophin actin binding domain." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624459.

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Coriati, Adèle. "Skeletal Muscle Specific IRES Activity of Utrophin A Is Enhanced by Eef1a2." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19866.

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Understanding the regulatory mechanisms controlling utrophin A expression at the sarcolemma of dystrophic muscles will facilitate the development of therapeutic strategies to ameliorate the pathophysiological features of Duchenne Muscular Dystrophy (DMD). The main goal of this study was to characterize the regulation of utrophin A IRES activity using a transgenic mouse model expressing the utrophin A 5’UTR bicistronic reporter and to identify trans-acting factors that could mediate IRES activity and endogenous expression of utrophin A. We found that utrophin A IRES activity is specifically exp
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8

Péladeau, Christine. "Utrophin A Upregulation by FDA-Approved Drugs for the Treatment of Duchenne Muscular Dystrophy." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39298.

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Duchenne Muscular Dystrophy (DMD) is a disorder caused by mutations in the dystrophin gene, preventing the production of the functional dystrophin protein which assures maintenance of the myofiber integrity throughout muscle contraction. A lack of dystrophin results in severe muscle degeneration and regeneration accompanied by a loss of muscle function. Many pre-clinical and clinical studies are focused on developing strategies to counteract the detrimental effects of DMD; however, there is no cure. One such approach consists of upregulating the endogenous protein utrophin A in dystrophic musc
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9

Perkins, Kelly Joanne. "Molecular and functional analysis of the transcriptional regulation of utrophin." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270259.

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Wilson, James Baillie. "Transcription of the utrophin gene : identification and characterisation of novel transcripts." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392667.

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Libros sobre el tema "Utrophin"

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Harrison, Mary-Ann. The molecular basis of Duchenne muscular dystrophy: Utrophin as a candidate for therapeutic intervention. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2004.

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Capítulos de libros sobre el tema "Utrophin"

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"Utrophin: The Intersection Between Pharmacological and Genetic Therapy." In Duchenne Muscular Dystrophy, 279–306. CRC Press, 2006. http://dx.doi.org/10.3109/9780849374456-15.

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"Utrophin in the Therapy of Duchenne M uscular D ystrophy." In Molecular Mechanisms of Muscular Dystrophies, 53–66. CRC Press, 2006. http://dx.doi.org/10.1201/9781498713962-8.

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Actas de conferencias sobre el tema "Utrophin"

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Bell, Brett J., and Sherry L. Voytik-Harbin. "Multiaxial Study of Fibroblast Biomechanics in a 3D Collagen Matrix." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206722.

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It is becoming increasingly evident, that of the signaling modalities relevant to the cell-extracellular matrix (ECM) microenvironment, the mechanical component is a very important mediator of cell behavior (reviewed in [1, 2]). Indeed, proliferation, ECM protein expression (collagen), matrix metalloproteinase (MMP) levels, migration, and stem cell differentiation, have all been shown to be affected by mechanical environmental cues [3, 4]. Although the importance of physical signaling mechanisms has been well established, the bulk of this work has yet to be translated to a more physiologic 3D
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2

Eldor, A., M. Bar-Ner, L. Wasserman, Y. matzner, Z. Fuks, and I. Viodavsky. "HEPARIN AND NON-ANTICOAGULANT HEPARINS INHIBIT HEPARANASE ACTIVITY IN NORMAL AND MALIGNANT CELLS:POSSIBLE THERAPEUTIC USE IN PREVENTION OF EXTRAVASATION AND DISSEMINATION OF BLOOD BORNE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643664.

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Degradation of vascular subendothelium occurs in_vivo during the process of inflammation and tumor invasion. Various observations suggest that the capacity of some blood-borne cells to extravasate may depend in part on their ability to express hepara-nase activity. Incubation of human platelets, human nc-utrophils, or highly metastatic mouse lymphoma cells with sulfate-labeled extracellular matrix (ECM) results in heparanase mediated release of labeled heparan sulfate cleavage fragments (0.5<Kav<0.85 on Sepharose 5B) (J. Clin.Invest. 74: 1842 and 76: 1306; Cancer Res. 43: 2704). The pres
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