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You searched for subject:(embryonic myosin). Showing records 1 – 2 of 2 total matches.

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University of Colorado

1. Vera, Carlos D. Functional Characterization of Disease-Causing Mutations in Human Myosin Heavy Chain Genes.

Degree: PhD, 2018, University of Colorado

Biophysical and biochemical imbalance of mechanisms relevant to muscle function, can result in morphological changes to the tissue. While the purpose of activities involving exercise is to modify the shape and size of skeletal muscle, and the length of these muscles allows wide ranges of stiffness and stretch to be applied, cardiac tissue is not meant to change much. However, stressful extrinsic factors (poor diet, chemotherapy, etc) or intrinsic factors like inherited mutations in muscle functioning genes can result in a myopathy or a disease of the muscle. In fact, another biological process that requires much compliance of many molecules is embryogenesis. Although the timeline of an embryonic structure is limited, compared to an adult heart and muscle composition, continuous and coordinated movement is essential, but cumulative, prolonged disruptions can be harmful. At the core of muscle biology is the myosin molecule which is a motor protein that hydrolyzes ATP, binds to actin, and the spatial dynamics of its function (contraction-relaxation) alter the length of muscle. Myosin cyclically follows specific steps and undertakes well-defined structural conformations during these events, but mutations can alter the time and stability of any of these aspects. In this thesis I did a comprehensive analysis of the ATPase cycle parameters for both embryonic and cardiac myosin and studied the effects of specific associated or linked mutations have on function. The multiple mutations were in the interest of cataloging common features and defects to identify mechanistic patterns. In a collaborative effort I also used these wet-lab measurements to simulate the cycle using a working kinetic model for the myosin ATPase cycle. We have found distinct differences between three different myopathies that will be discussed in the following chapters. Advisors/Committee Members: Leslie A. Leinwand, Thomas Perkins, Andreas Hoenger, Michael Stowell, Hector Rodriguez.

Subjects/Keywords: cardiomyopathy; muscle; myosin; embryonic myosin; atpase cycle parameters; Biochemistry; Biophysics; Molecular Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Vera, C. D. (2018). Functional Characterization of Disease-Causing Mutations in Human Myosin Heavy Chain Genes. (Doctoral Dissertation). University of Colorado. Retrieved from https://scholar.colorado.edu/mcdb_gradetds/94

Chicago Manual of Style (16th Edition):

Vera, Carlos D. “Functional Characterization of Disease-Causing Mutations in Human Myosin Heavy Chain Genes.” 2018. Doctoral Dissertation, University of Colorado. Accessed January 25, 2020. https://scholar.colorado.edu/mcdb_gradetds/94.

MLA Handbook (7th Edition):

Vera, Carlos D. “Functional Characterization of Disease-Causing Mutations in Human Myosin Heavy Chain Genes.” 2018. Web. 25 Jan 2020.

Vancouver:

Vera CD. Functional Characterization of Disease-Causing Mutations in Human Myosin Heavy Chain Genes. [Internet] [Doctoral dissertation]. University of Colorado; 2018. [cited 2020 Jan 25]. Available from: https://scholar.colorado.edu/mcdb_gradetds/94.

Council of Science Editors:

Vera CD. Functional Characterization of Disease-Causing Mutations in Human Myosin Heavy Chain Genes. [Doctoral Dissertation]. University of Colorado; 2018. Available from: https://scholar.colorado.edu/mcdb_gradetds/94

2. Humphrey, Peter Saah. Signal Transduction Mechanisms for Stem Cell Differentation Into Cardiomyocytes .

Degree: 2009, University of Hertfordshire

Cardiovascular diseases are among the leading causes of death worldwide and particularly in the developed World. The search for new therapeutic approaches for improving the functions of the damaged heart is therefore a critical endeavour. Myocardial infarction, which can lead to heart failure, is associated with irreversible loss of functional cardiomyocytes. The loss of cardiomyocytes poses a major difficulty for treating the damaged heart since terminally differentiated cardiomyocytes have very limited regeneration potential. Currently, the only effective treatment for severe heart failure is heart transplantation but this option is limited by the acute shortage of donor hearts. The high incidence of heart diseases and the scarcity donor hearts underline the urgent need to find alternative therapeutic approaches for treating cardiovascular diseases. Pluripotent embryonic stem (ES) cells can differentiate into functional cardiomyocytes. Therefore the engraftment of ES cell-derived functional cardiomyocytes or cardiac progenitor cells into the damaged heart to regenerate healthy myocardial tissues may be used to treat damaged hearts. Stem cell-based therapy therefore holds a great potential as a very attractive alternative to heart transplant for treating heart failure and other cardiovascular diseases. A major obstacle to the realisation of stem cell-based therapy is the lack of donor cells and this in turn is due to the fact that, currently, the molecular mechanisms or the regulatory signal transduction mechanisms that are responsible for mediating ES cell differentiation into cardiomyocytes are not well understood. Overcoming this huge scientific challenge is absolutely necessary before the use of stem cell-derived cardiomyocytes to treat the damaged heart can become a reality. Therefore the aim of this thesis was to investigate the signal transduction pathways that are involved in the differentiation of stem cells into cardiomyocytes. The first objective was the establishment and use of cardiomyocyte differentiation models using H9c2 cells and P19 stem cells to accomplish the specific objectives of the thesis. The specific objectives of the thesis were, the investigation of the roles of (i) nitric oxide (ii) protein kinase C (PKC), (iii) p38 mitogen-activated protein kinase (p38 MAPK) (vi) phosphoinositide 3-kinase (PI3K) and (vi) nuclear factor-kappa B (NF-kB) signalling pathways in the differentiation of stem cells to cardiomyocytes and, more importantly, to identify where possible any points of convergence and potential cross-talk between pathways that may be critical for differentiation to occur. P19 cells were routinely cultured in alpha minimal essential medium (??-MEM) supplemented with 100 units/ml penicillin /100 ??g/ml streptomycin and 10% foetal bovine serum (FBS). P19 cell differentiation was initiated by culturing the cells in microbiological plates in medium containing 0.8 % DMSO to form embryoid bodies (EB). This was followed by transfer of EBs to cell culture grade dishes after four…

Subjects/Keywords: Akt; Protein Kinase B; Bisindolylmaleimide I; 8-Bromo-cGMP; Caffeic Acid Phenethyl Ester; CAPE; Cardiomyocytes; Differentiation; Embryonic Stem Cells; H9c2 (2-1); Ly294002; Myosin Chain Light Chain 1; MLC; Myosin Heavy Chain; MHC; Nanog; Nitric Oxide; Nkx2.5; NOC-18; NOC-5; Nuclear Factor-Kappa B; NF-kB; P19 Embryonal Carcinoma Cell; P19 Stem Cells; P38 MAPK; P38 Mitogen-Activated Protein Kinase; Phosphoinositide 3-Kinase; PI3K; Protein Kinase C; PKC; SB203580; Signal Transduction; Signalling; SIN-1; SNAP; Sox2; Transcription Factors; Troponin I; Wnt Proteins; GATA; Bone Morphogenetic Proteins; Leukaemia Inhibitory Factor; Oct-4; Octamer-Binding Protein

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Humphrey, P. S. (2009). Signal Transduction Mechanisms for Stem Cell Differentation Into Cardiomyocytes . (Thesis). University of Hertfordshire. Retrieved from http://hdl.handle.net/2299/3760

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Humphrey, Peter Saah. “Signal Transduction Mechanisms for Stem Cell Differentation Into Cardiomyocytes .” 2009. Thesis, University of Hertfordshire. Accessed January 25, 2020. http://hdl.handle.net/2299/3760.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Humphrey, Peter Saah. “Signal Transduction Mechanisms for Stem Cell Differentation Into Cardiomyocytes .” 2009. Web. 25 Jan 2020.

Vancouver:

Humphrey PS. Signal Transduction Mechanisms for Stem Cell Differentation Into Cardiomyocytes . [Internet] [Thesis]. University of Hertfordshire; 2009. [cited 2020 Jan 25]. Available from: http://hdl.handle.net/2299/3760.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Humphrey PS. Signal Transduction Mechanisms for Stem Cell Differentation Into Cardiomyocytes . [Thesis]. University of Hertfordshire; 2009. Available from: http://hdl.handle.net/2299/3760

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

.