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Dissertations / Theses on the topic 'Muscle proteins'

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Published: 4 June 2021

Last updated: 1 August 2024

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1

Yost, John. "Influence of selection for breast muscle mass on pH and metabolism of supracoracoideus muscle from male and female turkey." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=892.

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Thesis (M.S.)--West Virginia University, 1999.
Title from document title page. Document formatted into pages; contains viii, 81 p. : ill. Vita. Includes abstract. Includes bibliographical references.

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2

Tomc, Lyn Kathryn. "Role of MEF2 proteins in the activation of the c-jun and MCK genes in skeletal muscle /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ56210.pdf.

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3

Vlahovich, 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.

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Cells contain an elaborate cytoskeleton which plays a major role in a variety of cellular functions including: maintenance of cell shape and dimension, providing mechanical strength, cell motility, cytokinesis during mitosis and meiosis and intracellular transport. The cell cytoskeleton is made up of three types of protein filaments: the microtubules, the intermediate filaments and the actin cytoskeleton. These components interact with each other to allow the cell to function correctly. When functioning incorrectly, disruptions to many cellular pathway have been observed with mutations in various cytoskeletal proteins causing an assortment of human disease phenotypes. Characterization of these filament systems in different cell types is essential to the understanding of basic cellular processes and disease causation. The studies in this thesis are concerned with examining specific cytoskeletal tropomyosin-defined actin filament systems in skeletal muscle. The diversity of the actin filament system relies, in part, on the family of actin binding proteins, the tropomyosins (Tms). There are in excess of forty Tm isoforms found in mammals which are derived from four genes: α, β, γ and δTm. The role of the musclespecific Tms in striated muscle is well understood, with sarcomeric Tm isoforms functioning as part of the thin filament where it regulates actin-myosin interactions and hence muscle contraction. However, relatively little known about the roles of the many cytoskeletal Tm isoforms. Cytoskeletal Tms have been shown to compartmentalise to form functionally distinct filaments in a range of cell types including neurons (Bryce et al., 2003), fibroblasts (Percival et al., 2000) and epithelial cells (Dalby-Payne et al., 2003). Recently it has been shown that cytoskeletal Tm, Tm5NM1 defines a cytoskeletal structure in skeletal muscle called the Z-line associated cytoskeleton (Z-LAC) (Kee et al., 2004).The disruption of this structure by over-expression of an exogenous Tm in transgenic mice results in a muscular dystrophy phenotype, indicating that the Z-LAC plays an important role in maintenance of muscle structure (Kee et al., 2004). In this study, specific cytoskeletal Tms are further investigated in the context of skeletal muscle. Here, we examine the expression, localisation and potential function of cytoskeletal Tm isoforms, focussing on Tm4 (derived from the δ- gene) and Tm5NM1 (derived from the γ-gene). By western blotting and immuno-staining mouse skeletal muscle, we show that cytoskeletal Tms are expressed in a range of muscles and define separate populations of filaments. These filaments are found in association with a number of muscle structures including the myotendinous junction, neuromuscular junction, the sarcolemma, the t-tubules and the sarcoplasmic reticulum. Of particular interest, Tm4 and Tm5NM1 define cytoskeletal elements in association with the saroplasmic reticulum and T-tubules, respectively, with a separation of less than 90 nm between distinct filamentous populations. The segregation of Tm isoforms indicates a role for Tms in the specification of actin filament function at these cellular regions. Examination of muscle during development, regeneration and disease revealed that Tm4 defines a novel cytoskeletal filament system that is orientated perpendicular to the sarcomeric apparatus. Tm4 is up-regulated in both muscular dystrophy and nemaline myopathy and also during induced regeneration and focal repair in mouse muscle. Transition of the Tm4-defined filaments from a predominsnatly longitudinal to a predominantly Z-LAC orientation is observed during the course of muscle regeneration. This study shows that Tm4 is a marker of regeneration and repair, in response to disease, injury and stress in skeletal muscle. Analysis of Tm5NM1 over-expressing (Tm5/52) and null (9d89) mice revealed that compensation between Tm genes does not occur in skeletal muscle. We found that the levels of cytoskeletal Tms derived from the δ-gene are not altered to compensate for the loss or gain of Tm5NM1 and that the localisation of Tm4 is unchanged in skeletal muscle of these mice. Also, excess Tm5NM1 is sorted correctly, localising to the ZLAC. This data correlates with evidence from previous investigations which indicates that Tm isoforms are not redundant and are functionally distinct (Gunning et al., 2005). Transgenic and null mice have also allowed the further elucidation of cytoskeletal Tm function in skeletal muscle. Analyses of these mice suggest a role for Tm5NM1 in glucose regulation in both skeletal muscle and adipose tissue. Tm5NM1 is found to colocalise with members of the glucose transport p fibres and analysis of both transgenic and null mice has shown an alteration to glucose uptake in adipose tissue. Taken together these data indicate that Tm5NM1 may play a role in the translocation of the glucose transport molecule GLUT4. In addition to this Tm5NM1 may play a role in adipose tissue regulation, since over-expressing mice found to have increased white adipose tissue and an up-regulation of a transcriptional regulator of fat-cell formation, PPAR-γ.

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4

Short, Kevin R. "Histochemical and biochemical changes in human muscle following 17 days of unilateral lower limb suspension." Virtual Press, 1997. http://liblink.bsu.edu/uhtbin/catkey/1063203.

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The present study was undertaken to determine the relationship between perinatal complications and subsequent development of Attention Deficit Hyperactivity Disorder (ADHD) and other behavioral characteristics. The biological mothers of 74 children diagnosed with ADHD and 77 children displaying no characteristics of the disorder completed the Maternal Perinatal Scale (MPS), the Behavior Assessment System for Children-Parent Rating Scales (BASC-PRS), and a demographic survey. In addition, the biological mothers of 120 children with no characteristics of ADHD or any other behavior disorders completed only the MPS so that exploratory factor analysis of the MPS could be completed.Following factor analysis, stepwise discriminant analysis of the resulting five factors was utilized to explore the nature of the relationship between such perinatal factors and ADHD. Results of this analysis indicated that emotional factors, or the amount of stress encountered during pregnancy and the degree to Relationship Between Perinatal Complications 3 was planned, were the items that maximized the separation between the ADHD and Non-ADHD groups. Additional discrimination between the groups was attributed to the extent of insult or trauma to the developing fetus and the outcome of prior pregnancies. ADHD children were also found to have experienced twice as many behavioral, social, or medical problems, and were more likely to reach developmental milestones with delays.Stepwise discriminant analysis also revealed the Attention Problems and Hyperactivity scales of the BASC-PRS were most significant in differentiating between the ADHD and Non-ADHD subjects. Using the BASC-PRS resulted in approximately 90% of the total sample being correctly classified as ADHD or Non-ADHD. Canonical correlation analysis indicated that emotional factors and the general health of both the mother and the developing fetus were the best predictors of later behavioral patterns reported on the BASC-PRS.
Human Performance Laboratory

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5

Vlahovich, Nicole. "The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease." View thesis, 2007. http://handle.uws.edu.au:8081/1959.7/32176.

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Thesis (Ph.D.)--University of Western Sydney, 2007.
A 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.

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6

Hodson, Elizabeth Anne Marie. "G protein regulation of phospholipase C in vascular smooth muscle." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390487.

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7

Jennison, Katy. "The electrical charge characteristics of muscle proteins." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304488.

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8

Hallett, Peter C. "Scanning force microscopy of striated muscle proteins." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296600.

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9

Newey, Sarah Elizabeth. "Functional analysis of #alpha#-dystrobrevin in muscle." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343522.

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10

Schuster, Joseph M. "The contribution of titin to striated muscle shortening." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/5758.

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Thesis (M.S.)--University of Missouri-Columbia, 2008.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. "December 2008" Includes bibliographical references.

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11

Tanner, Bertrand Clarke William. "Spatial coupling between sarcomeric proteins controls Ca2+-sensitive contraction muscle : a complementary research approach integrating theory with experiments /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/7995.

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12

Herron, Todd J. "Molecular regulation of power output in single rat skinned cardiac myocytes." MU has:, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3052177.

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13

Pacurari, Maricica. "Factors influencing crosslink formation in muscle tissue." Morgantown, W. Va. : [West Virginia University Libraries], 2001. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=2003.

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Thesis (M.S.)--West Virginia University, 2001.
Title from document title page. Document formatted into pages; contains ix, 86 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 70-86).

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14

Polikandriotis, John Anastasios. "Elucidating the regulation of vascular smooth muscle alpha-actin gene expression in fibroblasts." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1078857443.

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Thesis (Ph. D.)--Ohio State University, 2004.
Title from first page of PDF file. Document formatted into pages; contains xiv, 177 p.; also includes graphics (some col.). Includes bibliographical references (p. 160-177).

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15

Krammer, André Thomas. "Computational studies of protein-membrane interactions and forced unfolding of proteins /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/9697.

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16

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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17

Bryson, Elzbieta Anna. "Electrode measurement on the net charge on muscle proteins." Thesis, Open University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339914.

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18

Thongnuek, Peerapat. "The role of tendon matrix proteins in muscle adhesion." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709043.

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19

Gawalapu, Ravi Kumar Root Douglas. "Fluorescence labeling and computational analysis of the strut of myosin's 50 kDa cleft." [Denton, Tex.] : University of North Texas, 2007. http://digital.library.unt.edu/permalink/meta-dc-3974.

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20

Rowe, Tony. "Molecular dissection of myosin light chain function." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282103.

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21

Zhang, Jian Qiao. "Comparative studies with titin from tropical and temperate fish muscle." Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316940.

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22

McCloskey, Diana Teresa. "Adrenergic regulation of cardiac muscle contraction and relaxation." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324975.

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23

Satarug, Soisungwan. "Responses of skeletal muscle protein turnover and amino acid concentration to unloading, denervation and immobilization." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184308.

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The effects of denervation, non-weight bearing (unloading) or immobilization on hindlimb muscle growth, protein and amino acid metabolism were studied. In the first 3 days after denervation or unloading, atrophy of the soleus was caused by a suppression of protein synthesis and an acceleration of protein degradation. Thereafter, further atrophy, up to 6 days was due to depressed protein synthesis only. The changes in both protein synthesis and degradation in the first three days accounted for 69% and 65%, respectively, of the total loss of protein and mass in 6 days of unloaded or denervated soleus. Over the 6-day period, denervated soleus lost more mass and protein than the unloaded muscle owing to the earlier onset and greater extent of proteolysis. In denervated soleus, both lysosomal and non-lysosomal proteolysis may be enhanced, whereas in the unloaded muscle possibly only non-lysosomal proteolysis was enhanced. In both cases non-lysosomal proteolysis may be mediated by Ca²⁺-activated neutral protease, partially as a result of Ca²⁺ release from sarcoplasmic reticulum. Possibly due to the lack of lysosomal proteolysis, the insulin receptor did not show apparent increased turnover with unloading, as suggested by increased insulin sensitivity of in vitro protein turnover in the unloaded soleus. In contrast, denervated soleus showed a normal response to insulin for in vitro protein turnover. These findings suggested a mechanistic difference of unloading and denervation atrophy of soleus. A decreased ratio of glutamine/glutamate in fresh muscle suggested that the synthesis of glutamine in soleus may be diminished by denervation just as by unloading. This diminution of glutamine synthesis was probably due to reduced availability of ammonia, as evidenced by the slow disappearance of ATP in incubated denervated soleus. Similiar to unloading, denervation led to a decrease in aspartate concentration. This decreased concentration apparently resulted in decreased rather than increased utilization of aspartate. Effects of stretch on unloaded soleus were particularly pronounced in the first two days. Thereafter, in the stretched, unloaded soleus protein degradation increased to nearly the same extent as did protein synthesis. Hence after two days, stretch seems to lose its effectiveness in mitigating the effects of unloading so that it may not be an adequate preventive measure of muscle wasting under non-weight bearing condition.

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24

Lightfoot, Adam Paul. "Skeletal muscle as an endocrine organ : impact of muscle-derived cytokines and extracellular heat shock proteins." Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569584.

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Skeletal muscle wasting in the critically ill with sepsis is intrinsically linked to the elevations in circulating levels of cytokines characteristic to systemic inflammation and this effect may be exacerbated in older people. A key cytokine in this hyper- inflammatory state is TNF -a. Muscle is a plastic organ which adapts to stresses, including systemic inflammation in a number of ways, including the increased expression of Heat Shock Proteins (HSPs) and increased expression and release of cytokines (myokines). The release of HSPs by non-muscle cells has been described, but the extracellular function of HSPs is poorly understood. The aims of this thesis were to determine the effect of TNF-a on HSP and cytokine release by muscle; to elucidate the mechanism of HSP release from skeletal muscle, to identify the autocrine and paracrine signalling properties of eHSPs and to determine the impact of ageing on the ability of skeletal muscle to act as an endocrine organ. C2C12 myotubes were treated with TNF-a and cells and media were examined for HSP and cytokine content. The mechanisms of HSP and cytokine release were examined which included exosomal and golgi-mediated processes. The paracrine effects of muscle-derived HSP60 were determined by treatment of myotubes or SaOs-2 osteoblast cells with HSP60 at concentrations comparable to serum levels reported in critically ill patients. To determine the effect of TNF-a on the release of HSP60 and cytokines from muscles of old mice, isolated muscle fibres from the FDB of adult and old mice were treated with TNF-a. Treatment ofC2C12 myotubes with TNF-a resulted in increased content ofHSPlO, HSP60 and HSP70 and several cytokines. TNF-a treatment resulted in the specific release of HSP60 as well as IL-6, MCP-l, KC and RANTES from myotubes into the cell culture media. Inhibitor studies demonstrated that the release of HSP60 occurred via exosomes whereas cytokines were released by golgi-mediated transport. Treatment of myotubes with HSP60 resulted in the release of IL-6, MCP-l and RANTES by muscle cells but had no effect on markers of bone formation in SaOs-2 osteoblast cells. Treatment of C2C12 myotubes or SaOs-2 osteoblast cells with muscle-derived exosomes had no effect on cytokine release or markers of bone formation respectively. Comparison of the amount of JiSP60 released by muscle in exosomes to levels reported in pathological states sugpest that muscle is not a major source of HSP60. In contrast, comparison of the levels of cytokines released by muscle suggest that muscle is likely to be a major source of these cytokines in the critically ill. Treatment of isolated fibres from the FDB muscle of adult WT mice with TNF-a resulted in the significant increase in HSP60, IL-6 and KC in the media. In contrast, no effect was seen on the media content of HSP60 following treatment of isolated fibres from old WT mice although the media content of cytokines was comparable to that from fibres of adult WT mice. Data suggest that muscle can act as a significant source of cytokines in response to elevated levels of TNF -a and this may have significant implications for treatment of the critically ill. Muscle can release HSP60 as part of an exosomal process although the levels of HSP60 released are lower than those required to activate cytokine production and release by muscle or osteoblast cells. In contrast, muscle can act as a significant contributing source of cytokines in response to elevated levels of HSP60 derived from other cell types.

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25

Santos, Priscila Carvalho. "Efeitos do treinamento de força associado à suplementação de proteína e carboidrato na força e hipertrofia muscular de homens jovens destreinados /." Araraquara, 2017. http://hdl.handle.net/11449/151545.

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Orientador: Ellen Cristini de Freitas
Coorientador: Cleiton Augusto Libardi
Banca: Enrico Fuini Puggina
Banca: Hugo Tourinho Filho
Resumo: Sabe-se que o o treinamento de força (TF) promove aumento da massa muscular esquelética (i.e., hipertrofia muscular). Isso ocorre devido a frequentes aumentos na síntese proteica muscular (SPM) após cada sessão de TF. Quando a sessão de TF é sucedida pela ingestão de proteínas (PROT) de alto valor biológico, a SPM é ainda mais elevada, o que contribui também para maiores ganhos de força e massa muscular. Somado à esses efeitos, a associação do consumo de carboidrato (CHO) à PROT passou por especulações no campo científico, acreditando-se em efeitos aditivos do CHO nos processos de anabolismo muscular, além de mostrar-se determinante na recuperação muscular, como a ressíntese do glicogênio, que possui papel fundamental para a realização do exercício. Entretanto, esses achados foram investigados de forma aguda, fazendo-se necessário avaliar esses efeitos a longo prazo, visto que nem sempre as respostas agudas estão associadas as adaptações crônicas, ao menos no que diz respeito a hipertrofia muscular. Objetivo: Verificar o efeito da suplementação de PROT+CHO no VTT, hipertrofia e força muscular. Métodos: Participaram do estudo 22 indivíduos do sexo masculino, com idade entre 19 e 30 anos divididos em dois grupos: suplementação PROT e suplementação de PROT+CHO, os quais realizaram treinamento de força durante 8 semanas. A área de secção transversa muscular foi avaliada por meio de imagens de Ultrassonografia (US) e a força muscular através do teste de força máxima dinâmica (1RM... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Introduction: Is well know that resistance training (RT) promotes an increase in a fat free body mass (i.e. muscular hypertrophy). It is due to frequents increase in muscle protein synthesis (SPM) after each RT session. When RT session is succeeded by high biological value protein ingestion (PROT), SPM is much more elevated, which also contributes to greater gains in strength and muscle mass. In addition to those effects, the association of carbohydrate consumption (CHO) to PROT has been speculated in a scientific field, believing in additive effects of CHO in muscle anabolism process, besides being determinant in a muscle recuperation, like glycogen resynthesis, which has a fundamental role to exercise realization. However, those founds were investigated in acute intervention, being necessary to evaluate such effects in a long term study, since not always the acute responses are associated to chronic adaptations, at least related to muscle hypertrophy. Objective: To evaluate the effect of PROT+CHO supplementation on VTT, hypertrophy and muscle strength. Methods: Twenty-two male subjects, between 19 and 30 years, divided into two groups: PROT supplementation and PROT + CHO supplementation, who underwent strength training for 8 weeks, participated in the study. The muscle cross-sectional area was assessed using Ultrasonography (US) images and muscle strength through the maximal dynamic force (1RM) test. Results: No significant difference (p> 0.05) in VTT was found between the groups. The two groups showed significant increases in strength (PROT + CHO: 33.44%, PROT: 35.88%) and AST (PROT + CHO: 14.73%, PROT: 13.37%) after 8 weeks of intervention (Pre). Conclusions: The CHO + PROT supplementation did not promote additional effect on performance (VTT), muscle hypertrophy and strength gain, when compared to PROT supplementation... (Complete abstract click electronic access below)
Mestre

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26

Arden, Stuart Richard. "Functional properties of secreted proteins of muscle stage #Trichinella spiralis'." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309671.

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27

Osborn, Dan. "Regulation of myogenic bHLH proteins during zebrafish slow muscle development." Thesis, King's College London (University of London), 2008. https://kclpure.kcl.ac.uk/portal/en/theses/regulation-of-myogenic-bhlh-proteins-during-zebrafish-slow-muscle-development(80efc981-2fb8-47c3-a63b-8fd433f7f487).html.

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28

Green, Hannah Jane. "Diverse functions for intern associated proteins in Drosophila adult muscle." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/264024.

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The ability to adhere to the extracellular matrix (ECM) is critical for numerous cell types and tissues including epithelia and muscle. Cell-ECM adhesion is primarily mediated by integrins which provide a direct link between the ECM and the actin cytoskeleton. Integrin adhesions are frequently associated with a core of 60 different proteins (integrin-associated proteins, IAPs). Integrins are required for muscle attachment and in Drosophila, loss of integrins and several IAPs results in embryonic lethality and muscle detachment. However, the IAPs FAK, RSU1, tensin, vinculin and zyxin are not required for viability or embryonic muscle attachment. Furthermore, FAK, RSU1, tensin and vinculin have been observed to localise to muscle attachment sites in Drosophila, indicating that they have some function in muscle attachment. Unlike FAK, RSU1, tensin and vinculin, it was not previously known whether zyxin is expressed in Drosophila muscles. To test this, I generated a genomic zyxin-GFP construct that should contain most of the endogenous zyxin promotor. The genomic zyxin-GFP construct was not observed at muscle attachment sites, suggesting that it is not normally expressed in muscle. I wished to know whether FAK, RSU1, tensin and vinculin are required for muscle function. Various behavioural assays were employed to test for muscle function in larvae and adult flies. The results suggest that larval muscle function was normal in flies lacking these IAPs, but that adult muscle function might be impaired, although it proved difficult to demonstrate a clear functional defect. I then tested whether the IAPs FAK, RSU1, tensin and vinculin are required for normal morphology of adult muscles, focusing on the adult indirect flight muscles (IFMs). The IFMs are fibrillar muscles which attach to the cuticle via specialised epithelial cells known as tendon cells. At the end of the myofibril, where the myofibril attaches to the tendon cell, is a dense region of actin and IAPs known as the modified terminal Z-band (MTZ). I have found that the MTZ is not a homogenous zone of proteins, but is instead organised into at least three distinct layers. Because of the similarity between the structure of the MTZ with that of a hand, I refer to the layers as ‘fingers’, ‘palm’ and ‘wrist’. I discovered that the IAPs FAK, RSU1, tensin and vinculin are each required for the proper structure of the MTZ in unique ways. The fingers were elongated in IFMs lacking FAK, RSU1, tensin or vinculin, while the palm was disrupted in IFMs lacking RSU1, tensin or vinculin. Finally, I was intrigued by the enrichment of the actin-binding protein filamin/Cheerio in the palm and wished to know if it is required for palm function. Deletion of the C-terminus of filamin/Cheerio resulted in a reduction in palm length. Filamin/Cheerio is a mechanosensitive protein which exists in a closed and open conformation. I found that filamin/Cheerio must be open in order to help form a normal palm. Furthermore, vinculin is required to convert filamin/Cheerio from and closed to an open filamin/Cheerio state so that it can perform its function in the palm.

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29

Kasturi, Rama. "Kinetics of calmodulin binding to its smooth muscle target proteins /." The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487694702782747.

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30

Frei, Ryan. "Regulatory Elements of Drosophila Non-Muscle Myosin II." Thesis, University of Oregon, 2013. http://hdl.handle.net/1794/12954.

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Non-muscle myosin II (NM-II) is present in every cell type and moves actin filaments to provide contraction within the cell. NM-II has a motor domain, a neck domain that binds two light chains, a long coiled-coil tail domain, and a carboxyl-terminal tailpiece. NM-II forms bipolar filaments by associating near the carboxyl-terminus of the tail. It has long been known that both the formation of bipolar filaments and enzymatic activity of the motor domain are regulated by phosphorylation of one of the neck-binding light chains, known as the regulatory light chain (RLC). This phosphorylation causes a large-scale conformational shift of both the motor domains and the tail domain. However, the mechanism of this regulation and the elements that mediate the autoinhibition remain unknown. We have taken a deletional approach to finding the elements necessary for autoinhibition and regulation of filament assembly. We have used salt- dependent pelleting assays, cell culture, and analytical ultracentrifugation to identify two small regions in the IQ motifs of the neck and the carboxyl-terminal tailpiece that are essential for autoinhibition. Another necessary element for autoinhibition is the fold the coiled coil of the tail back on itself by means of hinge domains. We used internal deletions, pelleting assays, and thermal stability assays to identify and characterize the flexible hinge domains within the coiled-coil tail of NM-II. These hinges consist of low-stability regions of coiled coil, and can be stiffened by introducing mutations that cause the sequence to mimic a more ideal coiled coil. By defining these essential elements of autoinhibition, this work paves the way for a mechanistic understanding of the complex regulation of NM-II in the cell. This dissertation contains unpublished co-authored material.
2015-07-11

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31

Huang, Ping. "O-GlcNAc modification in muscle development." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/huang.pdf.

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32

Blagden, Christopher Simon. "The role of sonic hedgehog in slow muscle formation." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312763.

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33

Sjuve, Rolf. "Function of contractile and cytoskeletal proteins in smooth muscle effects of hypertrophy and age and of desmin removal in a transgenic animal /." Lund : Dept. of Physiology and Neuroscience, Lund University, 1998. http://books.google.com/books?id=ccFqAAAAMAAJ.

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34

Chen, Binbin. "Study of ID3 in the regulation of muscle creatine kinase gene expression." free to MU campus, to others for purchase, 1996. http://wwwlib.umi.com/cr/mo/fullcit?p9737883.

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Reidy, Paul T. "Influence of aerobic training on skeletal muscle protein composition." CardinalScholar 1.0, 2010. http://liblink.bsu.edu/uhtbin/catkey/1569026.

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Access to abstract permanently restricted to Ball State community only
Access to thesis permanently restricted to Ball State community only
School of Physical Education, Sport, and Exercise Science

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36

Aare, Sudhakar Reddy. "Intensive Care Unit Muscle Wasting : Skeletal Muscle Phenotype and Underlying Molecular Mechanisms." Doctoral thesis, Uppsala universitet, Klinisk neurofysiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-180374.

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Acute quadriplegic myopathy (AQM), or critical illness myopathy, is a common debilitating acquired disorder in critically ill intensive care unit (ICU) patients characterized by generalized muscle wasting and weakness of limb and trunk muscles. A preferential loss of the thick filament protein myosin is considered pathognomonic of this disorder, but the myosin loss is observed relatively late during the disease progression. In attempt to explore the potential role of factors considered triggering AQM in sedated mechanically ventilated (MV) ICU patients, we have studied the early effects, prior to the myosin loss, of neuromuscular blockade (NMB), corticosteroids (CS) and sepsis separate or in combination in a porcine experimental ICU model. Specific interest has been focused on skeletal muscle gene/protein expression and regulation of muscle contraction at the muscle fiber level. This project aims at improving our understanding of the molecular mechanisms underlying muscle specific differences in response to the ICU intervention and the role played by the different triggering factors. The sparing of masticatory muscle fiber function was coupled to an up-regulation of heat shock protein genes and down-regulation of myostatin are suggested to be key factors in the relative sparing of masticatory muscles. Up-regulation of chemokine activity genes and down-regulation of heat shock protein genes play a significant role in the limb muscle dysfunction associated with sepsis. The effects of corticosteroids in the development of limb muscle weakness reveals up-regulation of kinase activity and transcriptional regulation genes and the down-regulation of heat shock protein, sarcomeric, cytoskeletal and oxidative stress responsive genes. In contrast to limb and craniofacial muscles, the respiratory diaphragm muscle responded differently to the different triggering factors. MV itself appears to play a major role for the diaphragm muscle dysfunction. By targeting these genes, future experiments can give an insight into the development of innovative treatments expected at protecting muscle mass and function in critically ill ICU patients.

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37

Baranski, Alicia Michelle. "Regulation of somite myogenesis by cytokines occurs in specific somite regions and during distinct temporal periods /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/9244.

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38

Mei, Hua. "The role of G[alpha]z during muscle differentiation /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BICH%202006%20MEI.

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39

Sundaram, Priyanka. "The deubiquitinating enzyme USP19 negatively regulates the expression of muscle-specific genes in L6 muscle cells /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111547.

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Muscle wasting is a significant complication of many diseases including diabetes mellitus, renal and liver failure, HIV/AIDS, and cancer. Sustained loss of skeletal muscle can severely impair a patient's quality of life and often results in poor tolerance and responsiveness to disease treatments. The increased protein breakdown observed during muscle atrophy has been attributed to accelerated activity of the ubiquitin-proteasome pathway, but the precise mechanisms by which this activation stimulates muscle protein loss are poorly understood. Previous work showed that the deubiquitinating enzyme USP19 is upregulated in rat skeletal muscle in various forms of muscle wasting, including streptozotocin induced diabetes, cancer, and dexamethasone treatment. 1 To further explore the role of USP19 in muscle wasting, siRNA-mediated depletion of the enzyme was carried out in L6 myotubes. Knockdown of USP19 resulted in more rapid differentiation of myoblasts into myotubes, with a greater extent of myoblast fusion. It also produced tubes that were visibly larger than those formed by myoblasts transfected with a control siRNA. At the molecular level, silencing of USP19 increased the amount of myosin heavy chain (MHC) and tropomyosin proteins. It also increased levels of MHC transcript, suggesting that USP19 acts at the level of gene transcription or mRNA stability rather than protein degradation. USP19 may mediate its effects on muscle-specific gene expression through the myogenic transcription factor myogenin, since depletion of USP19 increased protein and mRNA levels myogenin but did not affect protein levels of the related transcription factor Myf5. Moreover, the increased tropomyosin and MHC observed upon USP19 knockdown could be abolished when myogenin was simultaneously depleted using siRNA. Collectively, these results suggest that USP19 functions to inhibit the synthesis of key muscle proteins and may therefore be a promising target for the treatment of muscle atrophy.

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40

Kirwan, Rochelle Dian. "Dietary protein versus supplemental protein in collegiate football athletes." Thesis, Montana State University, 2008. http://etd.lib.montana.edu/etd/2008/kirwan/KirwanR0808.pdf.

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Purpose: The purpose of this study was to determine if muscle hypertrophy and strength gains in athletes can be equally attained through dietary protein intake versus protein supplementation. Methods: Performance measures, body composition, and blood lipids were compared in redshirt football players who completed an eleven week protocol of either protein supplementation (S, n=6, 28 grams 3x/week) versus whole food protein (NS, n=9, 8-28 grams 3x/week). Subjects completed two 3-day diet records to determine nutrient intake. Results: Both groups reported meeting their protein requirements, but caloric intake was below the recommendation. Similar increases (P=0.003) in lean body mass were measured in the S (pre 72.2 Â± 6.6, post 73.0 Â± 6.3 kg) and NS groups (69.3 Â± 8.6, post 70.9 Â± 8.8 kg). No significant differences were found between the two groups in performance variables. For example, bench press increased (P=0.01) from 251 Â± 32 to 264 Â± 36 pounds in the S group and from 245 Â± 26 to 256 Â± 28 in the NS group. Conclusion: Both S and NS groups consumed on average at least the recommended protein intake and protein supplementation did not offer any performance or anabolic advantage over whole food protein.

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41

Van, der Giessen Kate. "Characterization of the role and regulation of the RNA binding protein HuR in muscle cell differentiation." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103304.

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Differentiation is the process of regulated gene expression that gives rise to different phenotypes from a common genotype. Skeletal muscle differentiation, myogenesis, is a good example of this process. Skeletal muscle is susceptible to injury due to direct or indirect causes. If left unrepaired, these injuries may lead to a loss of muscle mass, locomotive deficiency, and even lethality. Thus, understanding the molecular mechanisms behind this process is an important first step in the design of treatment for muscle-related diseases. Once myogenesis is induced, the expression of MRF proteins, such as MyoD and myogenin, is maintained at high levels in myofibers without the need to increase their rates of transcription, suggesting a role for post-transcriptional regulatory mechanisms. HuR is a ubiquitously expressed member of the embryonic lethal, abnormal vision (ELAV) family of RNA binding proteins that is known to post-transcriptionally regulate its target messages. Here, I demonstrate that, in the C2C12 muscle cell line, HuR is a required factor for both the initiation and maintenance of the myogenic process. First in vitro RNA Electro-Mobility Shift Assays (REMSA) and immunoprecipitation experiments demonstrated that HuR specifically binds to the AU-rich elements (AREs) that are present in the 3' untranslated regions (3'UTRs) of the MyoD and myogenin mRNAs. In the absence of HuR at the time of differentiation induction, accomplished using the siRNA technology, the expression of the MyoD and myogenin messages is significantly reduced, leading to inhibition of myogenesis. At this early stage in the differentiation process, HuR, a shuttling protein, is predominantly nuclear; localization that is mediated by the import receptor Transportin2 (Trn2). Nuclear HuR was determined to be required for the negative regulation of nucleophosmin (NPM) translation. Forced overexpression of NPM, resulting in differentiation inhibition, shows that its downregulation is a requirement for induction of the differentiation process. Late in myogenesis, however, NPM RNA is no longer expressed, and HuR is seen to accumulate in the cytoplasm of myotubes. This cytoplasmic accumulation results from dissociation of HuR from Trn2 due to caspase-dependent cleavage within its HNS region. Specifically blocking HuR import through the use of cell-permeable peptides, as well as RNAi-mediated depletion of Trn2, leads to an increase in cytoplasmic HuR, as well as increased cytoplasmic localization and stabilization of the MyoD and myogenin messages, and a corresponding enhancement of differentiation. Overall, we conclude that HuR is required for myogenesis due to its ability to post-transcriptionally regulate genes required for the process, and that HuR itself is regulated at the level of its subcellular localization, mediated by the import receptor TRN2.

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Altun, Mikael. "Old-age muscle atrophy: cellular mechanisms and behavioral consequences : an experimental study in the rat /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-305-4/.

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43

Banduseela, Varuna Chaminda. "Molecular And Cellular Networks in Critical Illness Associated Muscle Weakness : Skeletal Muscle Proteostasis in the Intensive Care Unit." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-183959.

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Critical illness associated muscle weakness and muscle dysfunction in intensive care unit (ICU) patients lead to severe morbidity and mortality as well as significant adverse effect on quality of life. Immobilization, mechanical ventilation, neuromuscular blocking agents, corticosteroids, and sepsis have been implicated as important risk factors, but the underlying molecular and cellular mechanisms remain unclear. A unique porcine ICU model was employed to investigate the effect of these risk factors on the expression profiles, gene expression and contractile properties of limb and diaphragm muscle, in the early phase of ICU stay. This project has focused on unraveling the underlying molecular and cellular pathways or networks in response to ICU and critical illness interventions. Upregulation of heat shock proteins indicated to play a protective role despite number of differentially transcribed gene groups that would otherwise have a negative effect on muscle fiber structure and function in response to immobilization and mechanical ventilation. Mechanical ventilation appears to play a critical role in development of diaphragmatic dysfunction. Impaired autophagy, chaperone expression and protein synthesis are indicated to play a pivotal role in exacerbating muscle weakness in response to the combined effect of risk factors in ICU. These results may be of therapeutic importance in alleviating critical illness associated muscle weakness.

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44

Leong, Peng Khun. "Complex interactions between skeletal muscle ryanodine receptor and dihydropyridine receptor proteins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0006/NQ41206.pdf.

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45

Ouellet, Marc. "Phosphocreatine-dependent phosphorylation of two cytosolic proteins in rat skeletal muscle." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60503.

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Phosphocreatine was found to alter the phosphorylation state of two proteins of apparent molecular weight 18 and 29 Kd when added to dialysed, cell-free extracts of rat skeletal muscle and brain, in the presence of $ lbrack tau$-$ sp{32}$P) ATP. The 29 Kd protein was identified as phosphoglycerate mutase. Phosphoglycerate mutase was phosphorylated at the active site histidyl residue by (2-$ sp{32}$P) 2,3-bisphosphoglycerate. 2,3-bisphosphoglycerate was labelled through the concerted action of phosphoglycerate kinase and 2,3-bisphosphoglycerate mutase. Phosphocreatine-dependent phosphorylation at this site resulted from a shift in phosphoglycerate kinase equilibrium, in the presence of creatine kinase, ultimately resulting in an increase in available (2-$ sp{32}$P) 2,3-bisphosphoglycerate. Maximal catalytic activity of phosphoglycerate mutase was not affected by phosphocreatine. These results suggest that phosphocreatine is unlikely to be important in regulating the activity of phosphoglycerate mutase in normal muscle. Previous reports of 3-phosphoglycerate-dependent protein phosphorylations, attributed to the action of novel kinases, are probably phosphoenzyme intermediates phosphorylated in a similar manner.

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46

Whytock, K. "An exploration into the proteins that regulate skeletal muscle lipid metabolism." Thesis, Liverpool John Moores University, 2019. http://researchonline.ljmu.ac.uk/9962/.

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Dysregulation of intramuscular triglyceride (IMTG) turnover in human skeletal muscle in sedentary and obese states leads to accumulation of lipid metabolites that contribute to skeletal muscle insulin resistance and ultimately progression to type 2 diabetes (T2D). People with T2D display low levels of IMTG turnover in comparison to insulin sensitive and trained individuals. IMTG stores are used as an energy substrate during 1 h of moderate-intensity exercise in trained individuals only and can be increased by consumption of a high fat, high calorie (HFHC) diet in sedentary and trained states. This thesis explores the metabolic and molecular regulation of proteins that regulate IMTG turnover, specifically focusing on the effects of 1) a HFHC diet and 2) a moderate-intensity exercise bout and 3) IMTG stores in different diseases states (lean, obese and T2D). Chapter 2 determined there were no sex-specific differences or main effects in functional outcomes of cardiovascular (arterial stiffness) and metabolic health (glucose tolerance and metabolic flexibility) in response to 7 days HFHC diet. Chapter 3 provides novel evidence that 7 days HFHC diet induces fibre type specific increases in IMTG stores primarily underpinned by an increase in perilipin-3 (PLIN3) protein expression and a redistribution of perilipin-2 (PLIN2) to lipid droplets (LD) storing IMTG. This occurred with no impairments in skeletal muscle insulin signalling and it is therefore proposed that increases in IMTG content assisted by PLIN2 and PLIN3 minimise the accumulation of lipid metabolites known to disrupt the insulin signalling cascade. Chapter 4 revealed that hormone sensitive lipase (HSL) preferentially redistributes to LD associated with perilipin-5 (PLIN5) following 1 h of moderate-intensity exercise. Chapter 5 developed a PLIN5 immunoprecipitation mass spectrometry protocol which identified phospholipase A2- group II, subgroup A (PA2GA) as a novel protein associated to PLIN5 in muscle from lean sedentary humans. In conclusion, this thesis presents novel data on key proteins that regulate IMTG turnover in human skeletal muscle.

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47

Haycock, John W. "Degradation of human muscle proteins by free radicals and proteolytic enzymes." Thesis, University of Newcastle upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260052.

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48

Sjekloca, Ljiljana. "Structural analysis of human striated muscle proteins: FATZ and γ-filamin." Doctoral thesis, SISSA, 2005. http://hdl.handle.net/20.500.11767/4670.

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The aim of the study we present in this PhD thesis is to gain a deeper insight into structure of Z-disc proteins FATZ 1 and y-filamin. Z-discs are multi-protein complexes which are the primary conduits of the force generated by striated muscle contraction. The protein composition of Z-disc is not well defined and new proteins are continuously being reported. FATZ 1 is expressed early during myofibrilogenesis and it is presumed to have an important role in Z-disc assembly and functioning. At the moment, it is the only Z-disc protein for which a direct connection with the signal transducer protein phosphatase calcineurin has been demonstrated. The protein sequence of FATZl does not account for its interaction with numerous proteins as it does not contain any known protein interaction domains. For this reason we investigated the structural characteristics of this Z-disc protein. We studied also y-filamin, a binding partner of FATZl. The role of filamins in cytoskeleton organization and signal transduction has been well documented. y-filamin is the muscle specific isoform of filamins and it has not been studied as extensively as other filamin isoforms. y-filamin can be found both at sarcolemma and at the Z-disc of striated muscle cells and for this reason is considered to be a structural and functional link between contractile apparatus and sarcolemma. y-filamin repeat 23 was reported to be necessary for the interaction of y-filamin and FATZ. We determined crystal structure of y-filamin repeat 23, and found that y-filamin repeat 23 bound nickel. Detailed analysis of y-filamin protein sequence indicated that other filamin repeats could bind nickel or similar divalent cations. Physiological importance of nickel in Eukaryotes is not well studied, but in Prokaryotes nickel is an essential component of many enzymes. Nickel binding to a protein with mainly structural role would be an exception, since nickel is bound mainly to proteins with enzymatic activities. We analyzed also structural characteristics of y-filamin repeat 20. The y-filamin repeat 20 has the unique muscle specific insertion responsible for protein localization in the Z-disc. The muscle specific insertion presents no homology with any sequence with known protein structure. Our results from structural studies of repeat 20 indicate that the insertion in repeat 20 influences the fold of this repeat and makes it structurally different from y-filamin repeat 23.

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Norman, Catalina. "Influence of the thin filament calcium activation on muscle force production and rate of contraction in cardiac muscle." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1178751966.

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50

Bergstrom, Donald Alan. "Orchestration of skeletal myogenesis by the myogenic bHLH family of transcription factors /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/6358.

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