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Articles 1 - 7 of 7
Full-Text Articles in Life Sciences
Loss Of The Na+/H+ Exchange Regulatory Factor 1 Results In Increased Susceptibility To Cisplatin-Induced Acute Kidney Injury., Adrienne M. Bushau-Sprinkle
Loss Of The Na+/H+ Exchange Regulatory Factor 1 Results In Increased Susceptibility To Cisplatin-Induced Acute Kidney Injury., Adrienne M. Bushau-Sprinkle
Electronic Theses and Dissertations
Background. Acute kidney injury (AKI), an abrupt loss of kidney function which carries a high mortality and confers an increased risk of chronic kidney disease, develops in 30% of patients who receive cisplatin, a widely used chemotherapeutic agent [1], [2], [3]. The sodium hydrogen exchange regulatory factor isoform 1 (NHERF1) is a scaffolding protein that anchors multiple membrane proteins, in renal proximal tubules [4]. NHERF-1 deficient mice have aberrant localization of BBM proteins in intracellular compartments [5]. The investigators have recently demonstrated NHERF1 deficient proximal tubule cells have an underlying …
Identifying The Signaling Mechanisms Of Egfr-Mediated Apoptosis., Nicole Marion Jackson
Identifying The Signaling Mechanisms Of Egfr-Mediated Apoptosis., Nicole Marion Jackson
Electronic Theses and Dissertations
The Epidermal Growth Factor Receptor (EGFR) is a 170-kilodalton transmembrane protein that belongs to the ErbB family of receptor tyrosine kinases. Upon ligand-mediated activation, the EGFR is responsible for cell growth, proliferation, and tissue homeostasis; however, the EGFR is overexpressed in many human malignancies, including MDA-MB-468 cells, a metastatic breast epithelial cell line. Studies within this cell line, and other cell lines characterized with high EGFR levels, have shown that EGF stimulation results in the induction of apoptosis. However, the mechanisms and signaling effectors implicated in this process have yet to be elucidated. The overarching research goal of this dissertation …
Tnf-Like Weak Inducer Of Apoptosis (Tweak) : Not So Weak After All., Joseph Dekward Mcmillan Iv
Tnf-Like Weak Inducer Of Apoptosis (Tweak) : Not So Weak After All., Joseph Dekward Mcmillan Iv
Electronic Theses and Dissertations
Background: Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a proinflammatory cytokine belonging to the TNF super family. TWEAK produces a variety of cellular responses through the binding to fibroblast growth factor inducible 14 (Fn14), a member of TNF receptor superfamily. Although Fn14 lacks a death domain, TWEAK has been found to induce apoptosis in some cell types by perturbing the activity of certain pathways such as TNF-receptor signaling. TWEAK is also known to regulate proliferation and differentiation of myogenic cells. We have previously reported that the TWEAK-Fn14 system causes skeletal muscle wasting both in vitro and in …
Modulation Of Cell Death Signaling And Cell Proliferation By The Interaction Of Homoserine Lactones And Paraoxonase 2., Aaron Mackallan Neely
Modulation Of Cell Death Signaling And Cell Proliferation By The Interaction Of Homoserine Lactones And Paraoxonase 2., Aaron Mackallan Neely
Electronic Theses and Dissertations
Pseudomonas aeruginosa produces N-(3-oxododecanoyl)-homoserine lactone (C12) as a quorum-sensing molecule that functions to facilitate bacteria-bacteria communication. C12 has also been reported to affect many aspects of human host cell physiology, including evoking cell death in various types of cells. However, the signaling pathway(s) leading to C12-triggerred cell death remains unclear. To clarify cell death signaling induced by C12, we examined mouse embryonic fibroblasts (MEFs) deficient in one or more caspases. Our data indicate that, unlike most apoptotic inducers, C12 evokes a novel form of apoptosis in cells, probably through the direct induction of mitochondrial membrane permeabilization. Previous studies indicate that …
Targeting The Anaphase Promoting Complex/Cyclosome To Induce Mitotic Arrest In Ovarian Cancer., Douglas John Saforo
Targeting The Anaphase Promoting Complex/Cyclosome To Induce Mitotic Arrest In Ovarian Cancer., Douglas John Saforo
College of Arts & Sciences Senior Honors Theses
Taxanes are a class of chemotherapeutic drug that act to disrupt microtubule function and cause mitotic arrest and cell death. These drugs are commonly used for cancer treatment, however their effectiveness is dependent on the presence of a functioning spindle assembly checkpoint (SAC). As a result, it is possible for cancer cells to become resistant to microtubule disrupting drugs by inactivating the SAC. The anaphase promoting complex/cyclosome (APC/C) is an E3 ubiquitin ligase that acts as the master regulator of cell cycle progression. Inhibition of the APC/C should result in disruption of the cell cycle, resulting in arrest during mitosis …
Mitochondria In Energy-Limited States: Mechanisms That Blunt The Signaling Of Cell Death, Steven C. Hand, Michael A. Menze
Mitochondria In Energy-Limited States: Mechanisms That Blunt The Signaling Of Cell Death, Steven C. Hand, Michael A. Menze
Michael Menze
Cellular conditions experienced during energy-limited states – elevated calcium, shifts in cellular adenylate status, compromised mitochondrial membrane potential – are precisely those that trigger, at least in mammals, the mitochondrion to initiate opening of the permeability transition pore, to assemble additional protein release channels, and to release pro-apoptotic factors. These proapototic factors in turn activate initiator and executer caspases. How is activation of mitochondria-based pathways for the signaling of apoptotic and necrotic cell death avoided under conditions of hypoxia, anoxia, diapause, estivation and anhydrobiosis? Functional trade-offs in environmental tolerance may have occurred in parallel with the evolution of diversified pathways …
Mitochondria In Energy-Limited States : Mechanisms That Blunt The Signaling Of Cell Death., Steven Hand, Michael Menze
Mitochondria In Energy-Limited States : Mechanisms That Blunt The Signaling Of Cell Death., Steven Hand, Michael Menze
Faculty Scholarship
Cellular conditions experienced during energy-limited states – elevated calcium, shifts in cellular adenylate status, compromised mitochondrial membrane potential – are precisely those that trigger, at least in mammals, the mitochondrion to initiate opening of the permeability transition pore, to assemble additional protein release channels, and to release pro-apoptotic factors. These proapototic factors in turn activate initiator and executer caspases. How is activation of mitochondria-based pathways for the signaling of apoptotic and necrotic cell death avoided under conditions of hypoxia, anoxia, diapause, estivation and anhydrobiosis? Functional trade-offs in environmental tolerance may have occurred in parallel with the evolution of diversified pathways …