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Characterization of FKGK18 as inhibitor of group VIA Ca2+-independent phospholipase A2 (iPLA2β): candidate drug for preventing beta-cell apoptosis and diabetesEvidence of contribution of iPLA2β-mediated events during islet β-cell apoptosis due to proinflammatory cytokines suggests a role for iPLA2β in T1D development.Regeneration of pancreatic non-β endocrine cells in adult mice following a single diabetes-inducing dose of streptozotocin.Inhibition of Ca2+-independent phospholipase A2β (iPLA2β) ameliorates islet infiltration and incidence of diabetes in NOD mice.Calcium-independent phospholipases A2 and their roles in biological processes and diseases.Gene transfer of active Akt1 by an infectivity-enhanced adenovirus impacts β-cell survival and proliferation differentially in vitro and in vivoGenetic modulation of islet β-cell iPLA₂β expression provides evidence for its impact on β-cell apoptosis and autophagyPolarization of Macrophages toward M2 Phenotype Is Favored by Reduction in iPLA2β (Group VIA Phospholipase A2)Impaired Store-Operated Calcium Entry and STIM1 Loss Lead to Reduced Insulin Secretion and Increased Endoplasmic Reticulum Stress in the Diabetic β-CellEndoplasmic reticulum stress alters ryanodine receptor function in the murine pancreatic β cell
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description
researcher ORCID ID = 0000-0003-3222-8918
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wetenschapper
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name
Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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Robert N Bone
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55209028100
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0000-0003-3222-8918