Open Access. Powered by Scholars. Published by Universities.®
Biomedical Engineering and Bioengineering Commons™
Open Access. Powered by Scholars. Published by Universities.®
- Keyword
- Publication Type
Articles 1 - 2 of 2
Full-Text Articles in Biomedical Engineering and Bioengineering
Gene Synthesis, Cloning, Expression, Purification And Biophysical Characterization Of The C2 Domain Of Human Tensin, Kiran Sukumar Gajula
Gene Synthesis, Cloning, Expression, Purification And Biophysical Characterization Of The C2 Domain Of Human Tensin, Kiran Sukumar Gajula
Doctoral Dissertations
Tensin is a large "docking" protein found in the adhesive junctions of animal cells and recruited early in the development of cell-substrate contacts. There it binds to the cytoplasmic domain of integrin β1 and caps the barbed ends of filamentous actin. This forms a rational basis for its implication in a direct role in the mechanics of membrane-cytoskeleton interactions. Tensin provides a physical link between the actin cytoskeleton, integrins, and other proteins at the cell-substrate contacts. Its overall biochemical properties are a function of its domain composition and architecture, i.e., the domains that are present and their relative positions in …
Resistance Of The Target Islet Tissue To Autoimmune Destruction Contributes To Genetic Susceptibility In Type 1 Diabetes., Natasha J. Hill, Aleksandr Stotland, Michelle Solomon, Patrick Secrest, Elizabeth Getzoff, Nora Sarvetnick
Resistance Of The Target Islet Tissue To Autoimmune Destruction Contributes To Genetic Susceptibility In Type 1 Diabetes., Natasha J. Hill, Aleksandr Stotland, Michelle Solomon, Patrick Secrest, Elizabeth Getzoff, Nora Sarvetnick
Journal Articles: Regenerative Medicine
Type 1 diabetes occurs when self-reactive T lymphocytes destroy the insulin-producing islet beta cells of the pancreas. The defects causing this disease have often been assumed to occur exclusively in the immune system. We present evidence that genetic variation at the Idd9 diabetes susceptibility locus determines the resilience of the targets of autoimmunity, the islets, to destruction. Susceptible islets exhibit hyper-responsiveness to inflammatory cytokines resulting in enhanced cell death and increased expression of the death receptor Fas. Fas upregulation in beta cells is mediated by TNFR2, and colocalization of TNFR2 with the adaptor TRAF2 in NOD beta cells is altered. …