The cell positions the working, counter, and reference electrodes and has an interior volume of approximately 200 mu l while simultaneously providing a full 1-cm path length for spectroscopic measurements. This method reduces the time required to perform a potentiometric titration on a molecule compared with standard chemical titration methods and achieves complete electrolysis of protein samples within minutes. Thus, the device combines the best aspects

of thin-layer cells and standard potentiometry. (C) 2013 Elsevier Inc. All rights reserved.”
“The tuberous sclerosis complex 2 (TSC2) gene encodes the protein tuberin, which functions as a key negative regulator of both mammalian target of rapamycin (mTOR) Cl-dependent cell growth and proliferation. Loss-of-function mutations selleck chemical of TSC2 result in mTORC1 hyperactivity and predispose individuals to both tuberous PF-04929113 sclerosis and lymphangioleiomyomatosis. These overlapping diseases have in common the abnormal proliferation of smooth muscle-like cells. Although the origin of these cells is unknown, accumulating evidence suggests that a metastatic mechanism may be involved, but the means by which the mTOR pathway contributes to this disease process remain poorly understood. In this

study, we show that tuberin regulates the localization of E-cadherin via an Akt/mTORC1/CLIP170-dependent, rapamycin-sensitive pathway. Consequently, Tsc2(-/-) epithelial cells display a loss of plasma membrane E-cadherin that leads to reduced cell-cell adhesion. Under confluent conditions, these cells detach, grow in suspension, and undergo AR-13324 datasheet epithelial-mesenchymal transition (EMT) that is marked by reduced expression levels of both E-cadherin and occludin and increased expression levels of both Snail and smooth muscle actin. Functionally, the Tsc2(-/-) cells demonstrate anchorage-independent growth, cell scattering, and anoikis resistance. Human renal angiomyolipomas and lymphangioleiomyomatosis

also express markers of EMT and exhibit an invasive phenotype that can be interpreted as consistent with EMT. Together, these results suggest a novel relationship between TSC2/mTORC1 and the E-cadherin pathways and implicate EMT in the pathogenesis of tuberous sclerosis complex-related diseases. (Am J Pathol 2010, 177:1765-177%. DOI: 10.2353/ajpath.2010.090233)”
“Advances in many aptamer-based applications will require a better understanding of how an aptamer’s molecular recognition ability is affected by its incorporation into a suitable matrix. In this study, we investigated whether a model aptamer system, the sulforhodamine B aptamer, would retain its binding ability while embedded in a multilayer polyelectrolyte film. Thin films consisting of poly(diallyldimethylammonium chloride) as the polycation and both poly(sodium 4-styrene-sulfonate) and the aptamer as the polyanions were deposited by the layer-by-layer approach and were compared to films prepared using calf thymus DNA or a random single-stranded oligonucleotide.