Mario Shields

Abstract The apical-basal polarity of pancreatic acinar cells is essential for maintaining tissue architecture. However, the mechanisms by which polarity proteins regulate acinar pancreas tissue homeostasis are poorly understood. Here, we evaluate the role of Par3 in acinar pancreas injury and homeostasis. While Par3 loss in the mouse pancreas disrupts tight junctions, Par3 loss is dispensable for pancreatogenesis.

Highlights • Loss of Gα13 in the KPC GEM model promotes pancreatic tumor development • Tumors from KPC mice with Gα13 loss demonstrate increased E-cadherin expression • Human pancreatic tumors with reduced Gα13 expression exhibit increased mTOR signaling • Gα13 loss sensitizes KPC tumors to rapamycin and reduces tumor growth in vivo Summary Gα13 transduces signals from G-protein-coupled receptors.

Abstract Programmed cell death or apoptosis is a central biological process that is dysregulated in many diseases, including inflammatory conditions and cancer. The detection and quantification of apoptotic cells in vivo is hampered by the need for fixatives or washing steps for non-fluorogenic reagents, and by the low levels of free calcium in diseased tissues that restrict the use of annexins.