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Full-Text Articles in Life Sciences
Identification Of Proteins Potentially Involved In The Formation Of Lafora Bodies, A Hallmark Of Lafora Disease, Elham Schokraie, Oliver Kötting, Matthew S. Gentry
Identification Of Proteins Potentially Involved In The Formation Of Lafora Bodies, A Hallmark Of Lafora Disease, Elham Schokraie, Oliver Kötting, Matthew S. Gentry
Molecular and Cellular Biochemistry Presentations
Lafora Disease (LD) is a fatal teenage-onset progressive myoclonus epilepsy. It is characterized by the formation of Lafora bodies (LBs), deposits of abnormally branched, insoluble, hyperphosphorylated glycogen-like polymers that are generally believed to trigger the development of the clinical symptoms of LD. 58% and 35% of the LD cases are caused by mutations in EPM2A (laforin) and EPM2B (malin), respectively. However, little is known about their function in LB formation. Two different mechanisms have been proposed to explain the accumulation of insoluble LBs: first, excessive glycogen phosphorylation and, second, an imbalance between glycogen synthesizing enzymes. The present study aims at …
Lysophosphatidic Acid Stimulates Lymphangiogenesis In Human Lymphatic Endothelial Cells, John Macbeth, Donna Nofziger-Plank
Lysophosphatidic Acid Stimulates Lymphangiogenesis In Human Lymphatic Endothelial Cells, John Macbeth, Donna Nofziger-Plank
Featured Research
Lymphangiogenesis is the process by which new lymphatic vessels sprout and grow from existing vessels whether under developmental, immunological, or cancerous conditions. Proper lymphatic vessel formation is important in working alongside normal angiogenesis in order to help regulate the body’s tissue fluid as well as aid in immunosurveillance. Various factors regulate lymphangiogenesis such as members of the vascular endothelial growth factor family (VEGF). Another factor that has recently been identified to play a role in lymphangiogenesis is the bio-active phospholipid lysophosphatidic acid (LPA) however the molecular mechanism by which LPA regulates lymphangiogenesis has not been well characterized. In this study, …
The Survivin And Ciap1 Anti-Apoptotic Proteins Are Differentially Downregulated In Response To Endoplasmic Reticulum Stress, Vicki Mercado, Jay L. Brewster
The Survivin And Ciap1 Anti-Apoptotic Proteins Are Differentially Downregulated In Response To Endoplasmic Reticulum Stress, Vicki Mercado, Jay L. Brewster
Featured Research
The endoplasmic reticulum (ER) is an organelle tasked with synthesis and transport of 50% of new cellular proteins. Dysfunction within this organelle creates signals for repair, adaptation, and in severe cases, cellular apoptosis. Multiple human diseases have been associated with ER dysfunction, and the activation of apoptosis in important populations of cells. Inhibitor of Apoptosis (IAP) proteins are cytosolic proteins that play an anti-apoptotic role in the cytosol. The relationship between endoplasmic reticulum (ER) stress and the expression/stability of IAPs is not well characterized. The objective of this study was to characterize the affect of ER stress on the expression/stability …
Evaluating Itpr-Dependence Of Apoptotic Signaling From The Endoplasmic Reticulum, Agustin Vargas, Jay L. Brewster
Evaluating Itpr-Dependence Of Apoptotic Signaling From The Endoplasmic Reticulum, Agustin Vargas, Jay L. Brewster
Featured Research
Stress within the endoplasmic reticulum (ER) can be induced by misfolded proteins accumulating in the lumen of this organelle. Signaling of ER stress to other parts of the cell results in altered gene expression, physiological adaptation, and with sustained stress, apoptosis (cell suicide). ER stress is often studied with highly toxic compounds that create severe ER stress rapidly, and a condition that is likely not physiologically relevant within an organism. In this study, we examine the apoptotic signaling induced by moderate ER stress, and in particular the inositol 1,4,5-trisphosphate receptor (ITPR). The ITPR regulates Ca2+ release from the ER lumen, …
Carbon Black And Titanium Dioxide Nanoparticles Differentially Activate Oxidative Stress And Apoptosis In A549 Human Alveolar Epithelial Cells, Sarah Alvarado, Brianna Manes, Jay L. Brewster
Carbon Black And Titanium Dioxide Nanoparticles Differentially Activate Oxidative Stress And Apoptosis In A549 Human Alveolar Epithelial Cells, Sarah Alvarado, Brianna Manes, Jay L. Brewster
Featured Research
Recent studies have demonstrated that variation between particulate matter compositions have universally adverse effects on cells and living tissues. Carbon black and titanium dioxide are two such particulates that we are continuously exposed to, yet there is limited research to examine the potential deleterious effects on living tissue. The objective of this study is to characterize the effect of carbon black (CB) and titanium dioxide (TiO2) particulates on A549 human alveolar epithelial lung cells. CB and TiO2 powders were dispersed throughout a solution of water and bovine serum albumin by high-powered sonication. The effects of these particulates on A549 cells …
The Regulatory Effect Of Semaphorin 7a On Proliferation And Migration In Human Umbilical Vein Endothelial Cells, Steven R. Flemming, Donna Nofziger-Plank
The Regulatory Effect Of Semaphorin 7a On Proliferation And Migration In Human Umbilical Vein Endothelial Cells, Steven R. Flemming, Donna Nofziger-Plank
Featured Research
Semaphorin 7A (SEMA 7A), a factor originally identified as regulating axon growth, has recently been implicated as a pro-angiogenic factor. The molecular mechanisms for this ability to stimulate angiogenesis have not been identified. This study examines if SEMA 7A can have a direct effect on vascular endothelial cells or whether it indirectly induces angiogenesis through stimulation and recruitment of macrophages as has been suggested. Using a human umbilical vein endothelial cells (HUVECs), the ability of SEMA 7A to affect proliferation and migration was examined. HUVECs were exposed to SEMA 7A directly or to conditioned media collected from macrophages exposed to …