Tomader Ali

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The present study investigated the role of selenium in the regulation of pancreatic beta-cell function. Utilising the mouse beta-cell line Min6, we have shown that selenium specifically upregulates Ipf1 (insulin promoter factor 1) gene expression, activating the -2715 to -1960 section of the Ipf1 gene promoter. Selenium increased both Ipf1 and insulin mRNA(More)
Among the family of phospholipases A2 (PLA2s) are the Ca(2+)-independent PLA2s (iPLA2s) and they are designated group VI iPLA2s. In relation to secretory and cytosolic PLA2s, the iPLA2s are more recently described and details of their expression and roles in biological functions are rapidly emerging. The iPLA2s or patatin-like phospholipases (PNPLAs) are(More)
Ongoing studies suggest an important role for iPLA2β in a multitude of biological processes and it has been implicated in neurodegenerative, skeletal and vascular smooth muscle disorders, bone formation, and cardiac arrhythmias. Thus, identifying an iPLA2βinhibitor that can be reliably and safely used in vivo is warranted. Currently, the mechanism-based(More)
β-cell apoptosis is a significant contributor to β-cell dysfunction in diabetes and ER stress is among the factors that contributes to β-cell death. We previously identified that the Ca²⁺-independent phospholipase A₂β (iPLA₂β), which in islets is localized in β-cells, participates in ER stress-induced β-cell apoptosis. Here, direct assessment of iPLA₂β role(More)
Type 1 diabetes (T1D) results from autoimmune destruction of islet β-cells, but the underlying mechanisms that contribute to this process are incompletely understood, especially the role of lipid signals generated by β-cells. Proinflammatory cytokines induce ER stress in β-cells and we previously found that the Ca(2+)-independent phospholipase A2β (iPLA2β)(More)
Autoimmune β-cell death leads to type 1 diabetes, and with findings that Ca(2+)-independent phospholipase A2β (iPLA2β) activation contributes to β-cell death, we assessed the effects of iPLA2β inhibition on diabetes development. Administration of FKGK18, a reversible iPLA2β inhibitor, to NOD female mice significantly reduced diabetes incidence in(More)
OBJECTIVES We wished to identify a major transcript that is upregulated during in vivo pancreatic islet neogenesis and examine the expression of the gene in beta and ductal cells. METHODS Differential display polymerase chain reaction was used to identify upregulated transcripts after islet neogenesis was stimulated in the rat by brief occlusion of the(More)
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