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Full-Text Articles in Entire DC Network
Prion Protein As An Infectious Agent Of Transmissible Spongiform Encephalopathies, Wioleta Cyranek
Prion Protein As An Infectious Agent Of Transmissible Spongiform Encephalopathies, Wioleta Cyranek
ETD Archive
Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases of human, animal and yeast caused by an infectious agent designated prion. The "protein only" hypothesis proposed more than three decades ago suggests that the prions are small, infectious pathogens composed of aggregated, abnormal forms of a protein encoded in the host genome. PrPC plays primary role in neurite outgrowth, synaptic function, oxidative stress defense and long term survival of cerebellar neurons. The key event in prion disease is the conversion of the Îł-helical, cellular isoform of the prion protein to the insoluble, Îø-sheet-rich disease- causing isoform. Aggregation of misfolded prion protein …
An Insight Into Gait Complex Mediated Translational Silencing, Purvi Kapasi
An Insight Into Gait Complex Mediated Translational Silencing, Purvi Kapasi
ETD Archive
Transcript-specific translational control restricts macrophage inflammatory gene expression. The pero-inflammatory cytokine IFN-Îđ induces the phosphorylation of human ribosomal protein L13a and its subsequent release from 60S ribosome. L13a is a component of the interferon-gamma-activated inhibitor of translation (GAIT). The GAIT complex binds a defined element in the 3'-untranslated region (UTR) of ceruloplasmin (Cp) mRNA and causes delayed silencing of translation. In this research, we elucidate the molecular mechanism underlying L13a translational silencing activity. L13a mediates translational silencing particularly, when driven by internal ribosome entry sites (IRESs) that requires the initiation factor eIF4G, but is resistant to silencing when driven by …
Optimization Of The Conditions Necessary To Show Binding Of The Plasmodium Yoelii Rhop-3 Rhoptry Protein To Mouse Erythrocytes, Latoya T. Myrie
Optimization Of The Conditions Necessary To Show Binding Of The Plasmodium Yoelii Rhop-3 Rhoptry Protein To Mouse Erythrocytes, Latoya T. Myrie
ETD Archive
The Plasmodium Rhop-3 rhoptry protein is an erythrocyte binding protein that is secreted into the RBC membrane during merozoite invasion. Anti-Rhop-3 antibodies inhibit merozoite RBC invasion. The C-terminus of the Rhop-3 protein is highly conserved among Plasmodium species and antisera from endemic areas reacts with recombinant C-terminus of Rhop-3. The binding domain of the Rhop-3 protein is hypothesized to be within the C-terminal region of the protein. In the present study I investigated the conditions necessary for binding of the Rhop-3 protein to RBC by expressing recombinant proteins made from partial fragments of the Rhop-3 gene using the vector pDisplayTM. …
Role Of Cd36 In Platelet Function, Arunima Ghosh
Role Of Cd36 In Platelet Function, Arunima Ghosh
ETD Archive
CD36 is a scavenger receptor expressed on a wide variety of cells including platelets. It recognizes multiple ligands, yet its function on platelets is incompletely characterized. Endothelial cell-derived microparticles (EMP) have been identified in diseases where platelet activation plays a pivotal role. Because EMP express phosphatidylserine (PS) on their surfaces, a CD36 ligand, we hypothesized that MP may bind to platelets via a PS-CD36 interaction. Human platelets were shown to bind EMP by flow cytometry and fluorescence microscopy. Binding was significantly inhibited by anti-CD36 antibody or using platelets from CD36 null donors. We observed a significant increase in the rate …
Temporal Activation Of The Jak-Stat Pathway In Relation To Cardiac Gene Expression In A Mouse Model Of Cardiac Dysfunction, Cassandra Talerico
Temporal Activation Of The Jak-Stat Pathway In Relation To Cardiac Gene Expression In A Mouse Model Of Cardiac Dysfunction, Cassandra Talerico
ETD Archive
Background: This project examined JAK-STAT pathway activation in two mouse models of cardiac hypertrophy: autoimmune myocarditis and pressure overload (PO). Methods: Myocarditis was induced with cardiac myosin PO was induced by transverse aortic constriction. STAT1, 3, and 5 binding was assessed by gel shift. STATs, JAKs, SERCA2A, and calsequestrin (CSQ) were quantified. In myocarditis, P-STAT3 localization to cardiac myocyte nuclei was ascertained, and plasma IL-6 and ventricular ANF mRNA were analyzed. Results: In myocarditis, STAT3/3 and STAT1/1 activation, inflammation, increased ventricle weight (P < 0.0001), and ANF mRNA (P = 0.005) occurred on days 14, 21, and 28. In PO, activation appeared on day 7 and persisted to failure. P-STAT3 increased (myocarditis, P < 0.0001 pressure overload, P < 0.05). P-JAK1 increased in myocarditis on days 21 and 28 (P < 0.007). In PO, CSQ and SERCA2A levels did not differ, but in myocarditis CSQ decreased (P = 0.02). In myocarditis, a biphasic elevation in plasma IL-6 occurred (P = 0.003). Conclusions: Although JAK-STAT signaling is activated in both models, it occurs earlier in PO and persists to heart failure, whereas in myocarditis it declines to basal levels as inflammation and plasma IL-6 return to baseline