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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Development of redox microphysiometry to assay cell signaling and metabolism /

Johnson, Jenifer L. January 2001 (has links)
Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 75-79).
2

Functional characterization of the split SET and MYND domain-containing methyltransferases, Smyd2 & Smyd3

Brown, Mark Alan, 1975- 28 August 2008 (has links)
Cell proliferation and differentiation are coordinated by synchronized patterns of gene expression. The regulation of these patterns is achieved, in part, through epigenetic mechanisms that affect the nature of DNA packaging into chromatin. Specifically, post-translational modifications to histone tails impact the structural dynamics of nucleosomes, thereby affecting DNA accessibility to transcriptional complexes. Accumulating evidence suggests that transcriptional regulators facilitate these alterations, resulting in altered local gene transcription. Thus, the structural interpretations of histone modifications are responsible for the establishment and maintenance of discrete programs of gene expression that ultimately correspond with distinct biological outcomes. Most histone lysine methyltransferases catalyze methyl transfer by way of the SET domain, a module encoded within many proteins that regulate diverse processes, including some critical for development and proper progression of the cell cycle. One such group of proteins, the SET and MYND domain (Smyd) family have been demonstrated to be direct regulators of tumorigenesis and essential developmental processes. Presented here is a functional characterization of two members of that family, Smyd2 and Smyd3. Smyd2 is identified as a member of the Smyd family and reported here to possess SET-dependent histone H3, lysine 36-specific methyltransferase activity. Smyd2 specifically associates with the Sin3A histone deacetylase complex, suggesting a link between two independent chromatin modification activities. Finally, over-expression of Smyd2 in fibroblasts is shown to significantly suppress their rate of growth. It is therefore proposed that Smyd2-mediated chromatin modifications regulate specific gene expression, thereby having important implications for normal and neoplastic cell proliferation. Aberrant expression of the histone H3-lysine 4-specific methyltransferase, Smyd3, has been implicated in colorectal, hepatocellular, and breast cell carcinogenesis. Here, Smyd3 is also shown to target histone H4, lysine 20 (H4K20). However, over-expression of Smyd3 in fibroblasts results in global reduction of trimethylation at H4K20 and this is accompanied by a striking increase in cell proliferation. As the methylation of H3K4 and H4K20 are normally associated with conflicting biological functions, I predict that these differential activities of Smyd3 are manifest under spatially and/or temporally distinct conditions, in the presence of different associating complexes, thereby resulting in effects that may be antagonistic of one another. / text
3

A modification of the method of Hewish and Burgoyne for the isolation of rat liver nuclei

Woll, Wesley George January 1980 (has links)
No description available.
4

Identification and characterization of a role for the actin cytoskeleton during sporulation in Saccharomyces cerevisiae

Davis, Dana Alan, 1969- January 1998 (has links)
The actin cytoskeleton is essential in yeast and is composed of actin and numerous actin binding proteins. One actin binding protein, encoded by SAC6, is the yeast homolog of human fimbrin, an actin bundling protein (1). Sac6 protein is not essential for viability but is involved in many cytoskeletal functions. One common phenotype cytoskeletal mutants, including the sac6Δ, have is a defect in sporulation. Although this phenotype has been known for some time, the function of the actin cytoskeleton during sporulation is completely unknown. In order to determine the role of Sac6 protein and the actin cytoskeleton for sporulation, I accomplished the following: (1) I identified the terminal arrest point of the sac6Δ during sporulation as being immediately prior to spore wall formation, (2) By analyzing other mutants, I established that a primary function for the cytoskeleton during sporulation is for endocytosis, and (3) I identified an endocytic pathway in vegetative cells having different requirements for the actin cytoskeleton than the classical endocytic pathway. The events occurring during sporulation have been characterized. By using a number of different assays, I determined that the sac6Δ arrests late in the sporulation pathway. Different arrest points were seen depending on strain background used. However, in the SK1 background, a function for Sac6 protein in spore wall formation was identified. By examining other mutations defective for sporulation, I identified sla2Δ and chc1-521 as having sporulation defects similar to the sac6Δ. SLA2 encodes a cytoskeletal protein that has roles in endocytosis and CHC1 encodes the clathrin heavy chain that has roles in membrane trafficking, including endocytosis (2-4). Actin and Sac6 protein are also required for endocytosis (5). These data led to the model that a function of the actin cytoskeleton during sporulation is for endocytosis. An allelic series of actin mutations had previously been analyzed for ability to undergo receptor-mediated endocytosis (6). This data was compared with the sporulation ability of the actin mutations and a strong correlation was identified between these two phenotypes. I determined that endocytosis does occur throughout sporulation and that the sac6Δ has defects in endocytosis during sporulation. In order to better understand the role of endocytosis during sporulation, I analyzed the endocytosis of Ste6 protein. The half-life of this protein is known to be controlled by the endocytic machinery and it is endocytosed constitutively (7). The data obtained from this assay (although not informative with regards to sporulation) suggests that Ste6 protein has different requirements for the actin cytoskeleton than receptor-mediated endocytosis. All endocytosis appears to require the actin cytoskeleton, however this may be the first demonstration that multiple actin-dependent endocytosis pathways may exist in yeast.
5

Addicted bodies cellular telephony, melancholia and individual articulation in Turkey /

Çelik Kutluay, Burçe. January 1900 (has links)
Thesis (Ph.D.). / Written for the Dept. of Art History and Communication Studies [Communications Graduate Program]. Title from title page of PDF (viewed 2008/07/29). Includes bibliographical references.
6

The mobile phone : a medium in itself /

Oksman, Virpi. January 1900 (has links) (PDF)
Thesis (doctoral)--University of Tampere, 2010. / Includes bibliographical references. Also available on the World Wide Web.
7

cdca8 : a target of p53/Rb dependent repression /

Jacob, Cara. January 2005 (has links)
Thesis (M.S.)--University of Toledo, 2005. / Typescript. "A thesis [submitted] as partial fulfillment of the requirements of the Master of Science degree in Biology." Bibliography: leaves 117-118.
8

Functional characterization of the split SET and MYND domain-containing methyltransferases, Smyd2 & Smyd3

Brown, Mark Alan, January 1900 (has links)
Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.
9

Identifying factors that promote tensional homeostasis in endothelial cells

Tam, Sze Nok 02 November 2017 (has links)
Various types of mammalian cells have an exceptional ability to adapt to externally applied mechanical stresses and strains. Because of this adaptation, cells can maintain their endogenous cytoskeletal stress at a preferred (homeostatic) state. This homeostasis of mechanical stress in cells, also known as tensional homeostasis, is essential for normal physiological functions of cells and tissues and provides protection against certain diseases. Recent experimental studies revealed a novel finding that isolated endothelial cells cannot maintain tensional homeostasis, whereas multicellular clusters can. Increasing size of the multicellular clusters played a critical role in attenuating temporal fluctuations of intracellular tension as it approached homeostasis. Here, we propose to interpret these experimental results with simple mathematical models and to gain insight into factors that contribute to homeostasis. The proposed models investigate solely on how mechanical interactions between cells influence tensional homeostasis and do not consider other physical and chemical factors such as biochemical signaling and substrate rigidity. Results of our model corroborated our earlier experimental findings that tensional homeostasis is multicellular phenomenon. We were able to identify two mechanisms that influence tensional homeostasis in confluent clusters, namely statistical averaging of stress fluctuations and stress buildup in the cluster that resulted from unbalanced portion of cell-substrate tractions at the cluster boundaries. To further investigate the role of cell-cell interactions in tensional homeostasis, we conducted traction measurements in thrombin-treated endothelial cells using micropatterned traction microscopy. Our expectation was that the presence of thrombin would stimulate cellular contractility to the point of severance of cell-cell adhesions. To our surprise, the cell-cell junctions remained intact. However, the measurements revealed a threshold in the cluster size after which attenuation in cellular tension rapidly progressed. The underlying mechanism that caused the presence of a threshold is still unknown. Current efforts of our research group are dedicated to reveal and understand those mechanisms.
10

From single cells to multicellular organisms : a quantitative analysis

Iber, Dagmar January 2006 (has links)
The evolution and development of multicellular organisms requires cells to differentiate, interact and "collaborate". Our understanding of the molecular mechanisms is still hazy. In this dissertation mathematical modelling is used to integrate available experimental data and to make testable predictions about such mechanisms. The thesis is split into three parts, each of which addresses one of the three challenges: differentiation, adhesion and collaboration. In the first part, a mathematical model is developed to explain how, in the absence of polarizing cues from the environment, sister cells with identical genomes can follow distinct routes of differentiation. It is shown that difference in cell size, resulting from asymmetric cell division, is sufficient to induce differential cell fate in Bacillus subtilis. The model predicts that this effect depends on the allosteric behaviour of a kinase and the low catalytic rate of the corresponding phosphatase; both properties were subsequently confirmed in experiments. During the development of multicellular organisms, differentiation can arise in response to gradients. By example of dorso-ventral patterning it is shown how a shallow maternal gradient can be converted into a sharp pattern. In the second part, a model for cell adhesion via integrins is developed, and it is shown that, for physiological parameters, binding of a ligand and of a stabilizing factor such as talin are insufficient for ligand-dependent integrin activation, and that a positive signaling feedback is required. In the final part, antibody affinity maturation is studied as an example for division of labour between collaborating cells. A novel B cell selection mechanism, based on competition for T cell help rather than for antigen, is proposed and shown to reconcile heretofore inexplicable experimental observations. Such a mechanism requires B cells to discriminate among different affinities of binding, and it is further shown that this can be achieved if B cell signaling is initiated by antigen-dependent receptor-inhibitor segregation. The predictions of the model match experimental measurements quantitatively.

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