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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.

Structure-function analysis of two Drosophila neuronal cell adhesion proteins fasciclin I and amalgam /

Liu, Xiao-yu. January 2007 (has links)
Thesis (Ph. D.)--Ohio State University, 2007.

The role of chemoattractants in modulating neutrophil-endothelial adhesion

Tan, Peter January 2000 (has links)
No description available.

A study of ion regulatory mechanisms in neural crest cells and fibroblasts

Dickens, Claire Julia January 1990 (has links)
No description available.

Investigation of the association of P13K with the cadherin-catenin adhesion complex

Woodfield, Richard John January 2000 (has links)
No description available.

Carcinoembryonic antigen (CEA) in the extrahepatic biliary tract : investigation of its function and localisation in benign and malignant epithelium

Maxwell, John Perry January 1997 (has links)
No description available.

Investigation of the role of N-acetylgalactosylated glycoconjugates in cancer metastasis using the lectin from Helix pomatia (the Roman snail)

Hall, Debbie M. S. January 2001 (has links)
No description available.

Chlamydia trachomatis, a cell adhesion architect : the role of TarP and CT228 in Chlamydia trachomatis modulation of host cell focal adhesions

Santos Tedim Sousa Pedrosa, António José January 2017 (has links)
Bacterial infection of mucosal epithelial cells triggers cell exfoliation to limit the dissemination of infection within the tissue. Therefore, mucosal pathogens must possess strategies to counteract cell extrusion in response to infection. Chlamydia trachomatis L2 spends most of its intracellular development in the non-infectious form, and premature extrusion of the host cell is detrimental to the pathogen. Here I show that Chlamydia trachomatis L2-infected cells exhibited increase adhesion as demonstrated by increased resistance to detachment by mild trypsinization. In addition, I observed an increase in the number and size of the focal adhesions of the Chlamydia trachomatis L2-infected cells. I demonstrated that this phenotype was not exclusive of C. trachomatis serovar L2 and that it was not restricted to a single type of cell line. Quantitative confocal and live-cell TIRF microscopy revealed that this bacterium actively modulated host cell focal adhesions by enhancing their stability. Infection conferred resistance to disassembly upon inhibition of myosin II or ROCK1 activity. Furthermore, I was able to demonstrate that the Chlamydia trachomatis effector TarP is able to colocalize to the sites of focal adhesions when ectopically expressed in mammalian cells. This resulted in increased number of the host cell focal adhesions. TarP was also able to confer resistance to myosin II inhibition, in a VBD-dependent manner. Also, I have found that C. trachomatis transmembrane protein CT228 cooperates with TarP to confer resistance to ROCK1 inhibition. Super resolution microscopy revealed a reorganisation of focal adhesions in Chlamydia trachomatis L2-infected cells. In summary, this work shows for the first time that Chlamydia trachomatis L2 uses TarP and CT228 to modulate the host cell focal adhesions. Finally, I have also described that both Chlamydia trachomatis L2 and TarP are able to alter the nanoscale architecture, this has never been reported in any other system.

Unique roles for the C3 gamma-protocadherin isoform in WNT signaling and dendrite arborization

Mah, Kar Men 01 December 2017 (has links)
A key component of neural circuit formation is the elaboration of complex dendritic arbors, the pattern of which constrains inputs to the neuron and thus, the information it processes. As such, many neurodevelopmental disorders such as autism and Down, Rett, and Fragile X Syndromes are associated with reduced forebrain dendrite arborization. Identifying molecules involved in regulating dendrite arborization and neural circuitry formation therefore, is a start to understanding these disorders. Nearly 70 cadherin superfamily adhesion molecules are encoded by the Pcdha, Pcdhb, and Pcdhg gene clusters. These so-called clustered protocadherins (Pcdhs) are broadly expressed throughout the nervous system, with lower levels found in a few non-neuronal tissues. Each neuron expresses a limited repertoire of clustered Pcdh genes, a complicated process controlled by differential methylation and promoter choice. The clustered Pcdh proteins interact homophilically in trans as cis-multimers, which has the potential to generate a combinatorially explosive number of distinct adhesive interfaces that may give neurons unique molecular identities important for circuit formation. Functional studies of animals in which clustered Pcdhs have been deleted or disrupted demonstrate that these proteins play critical roles in neuronal survival, axon and dendrite arborization, and synaptogenesis. Additionally, they have been implicated in the progression of several cancers, suggesting that basic studies of their function and signaling pathways will have important future clinical applications. Recent work has shown that γ-Pcdhs can regulate the Wnt signaling pathway, a common tumorigenic pathway which also play roles in neurodevelopment, but the molecular mechanisms remain unknown. I determined that γ-Pcdhs differentially regulate Wnt signaling: the C3 isoform uniquely inhibits the pathway while 13 other isoforms upregulate Wnt signaling. Focusing on γ-Pcdh-C3, I show that the variable cytoplasmic domain (VCD) is critical for Wnt signaling inhibition. γ-Pcdh-C3, but not other isoforms, physically interacts with Axin1, a key component of the canonical Wnt pathway. The C3 VCD competes with Dishevelled for binding to the DIX domain of Axin1, which stabilizes Axin1 at the membrane and leads to reduced phosphorylation of Wnt co-receptor Lrp6. I also present evidence that the Wnt pathway can be modulated up (by γ-Pcdh-A1) or down (by γ-Pcdh-C3) in the cerebral cortex in vivo, using conditional transgenic alleles. Studies have implicated γ-Pcdhs as a whole, in many neurodevelopmental processes but little is known if distinct roles exists for individual isoforms. By using a specific C3-isoform knockout mouse line engineered in collaboration with Dr. Robert Burgess of The Jackson Laboratory, I was able to uncover a unique role for the C3-isoform in the regulation of dendrite arborization. Mice without γ-Pcdh-C3 exhibit significantly reduced dendrite complexity in cortical neurons. This phenotype was recapitulated in cultured cortical neurons in vitro, which can be rescued by reintroducing the C3-isoform. The ability of γ-Pcdh-C3 to promote dendrite arborization cell-autonomously was abrogated when Axin1 was depleted with an shRNA, indicating that this process by which γ-Pcdh-C3 regulates dendrite arborization is mediated by its interaction with Axin1, which I had previously demonstrated. Together, these data suggest that γ-Pcdh-C3 has unique roles distinct from other γ-Pcdhs, in the regulation of Wnt signaling and dendrite arborization, both of which are mediated by interaction with Axin1.

Cell attachment to peplide modified glass surfaces.

Sinnappan, Snega Marina, Graduate School of Biomedical Engineering, Faculty of Engineering, UNSW January 2007 (has links)
Cell attachment is vital for the integration of biomaterials in the body. Surface modification using cell adhesive peptides, such as Arginine-Glycine-Aspartic (RGD), has showed promise for enhancing cell adhesion. Cell adhesion on glass and polyethylene glycol (PEGylated) surfaces modified with active RGD and Proline- Histidine-Serine-Arginine-Asparagine (PHSRN) peptides as well as inactive RDG and HRPSN control peptides was investigated in serum free conditions using three cell lines; NIH3T3 fibroblasts, MC3T3 pre-osteoblasts and C2C12 pre-myoblasts. Peptide attachment to glass surfaces was confirmed by x-ray photoelectron spectroscopy and contact angle measurements. Cell attachment and spreading was equivalent on all peptide and fibronectin coated glass surfaces and was significantly higher than on unmodified glass after 3 hours. Cell attachment to the peptide modified glass was reduced in the presence of soluble RGD and RDG peptides, indicating that cell attachment to these surfaces may be integrin mediated, but not specific for RGD. Inhibition of protein synthesis with cycloheximide revealed that endogenous protein synthesis did not influence the specificity of cell attachment to the peptide modified glass surfaces in all cell types within a 3 hour period. However, cycloheximide treatment inhibited cell spreading on the peptide modified glass surfaces, suggesting that proteins synthesis was required for spreading. Long term adhesion studies, within a 24 hour period, showed that all cell lines were able to remain attached to the peptide modified glass surfaces, while C2C12 and MC3T3 cells were also able to form focal adhesions during this period. Cell attachment to peptide modified PEGylated surfaces over a 3 hour period showed that NIH3T3 and C2C12 cells experienced significantly higher levels of cell attachment on the RGD modified surface compared to the other peptides. MC3T3 cells attached to all the peptide modified PEGylated surfaces to the same extent, suggesting that cell attachment to peptide modified PEGlyated surfaces, can be cell type dependent. In conclusion all the peptides were able to promote cell adhesion on glass surfaces in the absence of a PEG linker. In the presence of a PEG linker cellular response to the peptide surfaces was both peptide and cell type dependent.

Desmosomal and cytoskeletal protein interactions required for cell adhesion in human keratinocytes /

Smith, Elizabeth Anne. January 1999 (has links)
Thesis (Ph. D.)--University of Chicago, Dept. of Biochemistry and Molecular Biology, June 1999. / Includes bibliographical references. Also available on the Internet.

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