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

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1. Habela, Christa Whelan. Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes.

Degree: PhD, 2008, University of Alabama – Birmingham

The hypothesis that cell volume and the progression of the cell cycle are interdependent has surfaced off and on in the cell cycle literature for the past 30 years. However, a conclusion as to how cell volume is mechanistically involved in cell division has not been reached in mammalian cells. The aim of this dissertation was to establish how volume changes modulate cell cycle progression. Most of the studies addressing this question have examined mass content yet, more recently, focus has been placed on intracellular water, which is determined by the balance between mechanical and osmotic forces. As a result, ion channels and transporters which regulate intracellular osmotic content are integral to the maintenance of cell volume. In this dissertation, I show that a large, rapid and regulated volume decrease occurs as glioma cells progress through mitosis. I refer to this process as pre-mitotic condensation (PMC). This process is functionally linked to DNA condensation prior to cell division as the two events occur simultaneously, and inhibition of PMC results in a prolongation of DNA condensation. Further, my data demonstrates that glioma cells actively accumulate chloride, which acts as the primary energetic driving for cell volume changes in these cells. During the process of PMC, this gradient drives the efflux of chloride through ClC3 channels, which mediates water loss and the volume decrease. Interestingly, chloride accumulation to similar levels can be observed in immature astrocytes and neurons, suggesting that glioma cells recapitulate the biology of immature proliferating cells in the brain. This also suggests that my findings may have broader applicability to cell division in both neural cells and cancer.

xii, 132 p. : ill., digital, PDF file.

Neurobiology

Joint Health Sciences

Voltage Gated Chloride Channels Pre-miotic Condensation DND Condensation C1C3 Mitosis Volume Regulation

UNRESTRICTED

Advisors/Committee Members: Sontheimer, Harald, Bevensee, Mark<br>Engler, Jeffrey<br>Pozzo-Miller, Lucas<br>Theibert, Anne.

Subjects/Keywords: Cell Cycle  – physiology<; br>; Cell Movement  – physiology<; br>; Cell Proliferation<; br>; Cell Size<; br>; Chloride Channels  – physiology<; br>; Chlorides  – metabolism<; br>; Cytokinesis  – physiology<; br>; Glioma  – physiopathology<; br>; Mitosis  – physiology<; br>; Neuroglia  – physiology

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

APA (6th Edition):

Habela, C. W. (2008). Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,444

Chicago Manual of Style (16th Edition):

Habela, Christa Whelan. “Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 06, 2021. http://contentdm.mhsl.uab.edu/u?/etd,444.

MLA Handbook (7th Edition):

Habela, Christa Whelan. “Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes.” 2008. Web. 06 Mar 2021.

Vancouver:

Habela CW. Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2021 Mar 06]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,444.

Council of Science Editors:

Habela CW. Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,444

2. Cuddapah, Vishnu Anand. Regulation Of Clc-3 In Human Malignant Glioma.

Degree: PhD, 2012, University of Alabama – Birmingham

Malignant gliomas are the most common and deadly form of primary brain cancer afflicting adults. Current treatment regimens, including surgical debulking, radiotherapy, and chemotherapy, have limited efficacy, and median patient survival remains only 14 months. Therefore, novel therapies must target different aspects of glioma biology. Two of the most striking features of this cancer are the unusual ability of glioma cells to robustly proliferate and migrate in the brain, and recent evidence suggests that ClC-3, a voltage-gated Cl- channel/transporter is implicated in both of these processes. We hypothesize that ClC-3 may facilitate proliferation and migration by promoting hydrodynamic shape and volume changes; as Cl- efflux occurs, water osmotically leaves the cytoplasm. These shape and volume changes are critical as, for example, a glioma cell divides into 2 daughter cells, or migrates through narrow extracellular spaces in the brain. In this dissertation, we assess upstream signaling to determine how ClC-3 is activated in the context of proliferation and migration. Using a combination of biophysical, biochemical, genetic, and imaging techniques, we identify several mechanisms suggesting that Ca2+/calmodulin-dependent protein kinase (CaMKII) regulates ClC-3 activity. We demonstrate that channels or ligands that increase [Ca2+]i also activate CaMKII, leading to downstream ClC-3 activation and promoting proliferation and migration. CaMKII regulation of ClC-3 is required for a critical cytoplasmic condensation checkpoint at the metaphase-anaphase transition, and inhibition of either protein leads to disrupted volume regulation and proliferation. Additionally, we found that bradykinin, a chemotactic peptide, increases glioma cell migration by activating CaMKII-dependent ClC-3 channels. Inhibition of ClC-3 or CaMKII completely blocked bradykinin-induced migration. We propose that CaMKII activation of ClC-3 is a critical mediator of cellular proliferation and migration and should be integrated into preexisting models. We speculate that [Ca2+]i may be a ""master regulator"" of both proliferation and migration by simultaneously controlling cytoskeletal proteins, kinases, and Ca2+-sensitive ion channels. Finally, our data suggest that targeting Cl- channels or bradykinin receptors on human glioma cells may be a novel therapeutic strategy for the management of malignant gliomas.

PhD

1 online resource (xi, 213 p.) :ill., digital, PDF file.

Neurobiology

Joint Health Sciences

bradykinin cell migration chloride channel ClC-3 Cl- channel

UNRESTRICTED

Advisors/Committee Members: Harald Sontheimer, Bedwell,David Kirk,Kevin Nabors,Burt Wadiche,Jacques.

Subjects/Keywords: Brain Neoplasms – metabolism<; br>; Calcium-Calmodulin-Dependent Protein Kinase Type 2 – metabolism.<; br>; Cell Movement – physiology<; br>; Chloride Channels – metabolism.<; br>; Gene Expression Regulation<; br>; Gene Expression Regulation, Enzymologic<; br>; Gene Expression Regulation, Neoplastic<; br>; Glioma – metabolism<; br>; Ion Channels – metabolism<; br>; Membrane Transport Proteins – metabolism.<; br>; Mitosis<; br>; Neoplasms – metabolism<; br>; Neoplasms – pathology

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

APA (6th Edition):

Cuddapah, V. A. (2012). Regulation Of Clc-3 In Human Malignant Glioma. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1394

Chicago Manual of Style (16th Edition):

Cuddapah, Vishnu Anand. “Regulation Of Clc-3 In Human Malignant Glioma.” 2012. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 06, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1394.

MLA Handbook (7th Edition):

Cuddapah, Vishnu Anand. “Regulation Of Clc-3 In Human Malignant Glioma.” 2012. Web. 06 Mar 2021.

Vancouver:

Cuddapah VA. Regulation Of Clc-3 In Human Malignant Glioma. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2012. [cited 2021 Mar 06]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1394.

Council of Science Editors:

Cuddapah VA. Regulation Of Clc-3 In Human Malignant Glioma. [Doctoral Dissertation]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1394

.