Anti-AKT2 (aa 100-189) polyclonal antibody

Plant roots absorb potassium ions from the soil and transport them in the xylem via the transpiration stream to the shoots. There, in source tissues where sufficient chemical energy (ATP) is available, K+ is loaded into the phloem and then transported with the phloem stream to other parts of the plant; in part, transport is also back to the roots. This, at first sight, futile cycling of K+ has been uncovered to be part of a sophisticated mechanism that (1) enables the shoot to communicate its nutrient demand to the root, (2) contributes to the K+ nutrition of transport phloem tissues and (3) transports energy stored in the K+ gradient between phloem cytosol and the apoplast. This potassium battery can be tapped by opening AKT2-like potassium channels and then enables the ATP-independent energization of other transport processes, such as the reloading of sucrose. Insights into these mechanisms have only been possible by combining wetlab and dry-lab experiments by means of computational cell biology modeling and simulations.

Our study was to explore the potential role of miRNA-200b in modulating tumorigenesis in the model of ulcerative colitis-related colorectal cancer (UCRCC) and, further, to decipher the underlying mechanisms associated with this effect. In this study, we examined a greater number of polyps or adenomas, a higher grade of epithelial dysplasia accompanied with a decrease 'in survival ratio in azoxymethane (AOM)/dextran sulfate sodium (DSS) model mice compared to mice treated with over-expressed miRNA-200b. Surprisingly, enforced miRNA-200b expression significantly suppressed AOM/DSS-induced up-regulation of oncologic markers including A-catenin and CD133. Independent of this, treatment with miRNA-200b obviously attenuated inflammatory responses, as indicated by down-regulating tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-alpha) and blockade of AKT2-mediated NF-kappa B/IL-6/STAT3 signaling pathway. Furthermore, a simultaneous shift in epithelial-mesenchymal transition (EMT) markers such as E-cadherin and N-cadherin were observed to be increased and decreased, respectively. Coupled with the associated influence of over-expressed miRNA-200b were change in colorectal cell morphology shown by Transmission electron microscope (TEM) and a decrease in expression of rho-kinase2 (ROCK2) together with AKT2 phosphorylation (p-AKT2). Moreover, mice which were transfected with negative control of miRNA-200b possessed results that were in line with that obtained from AOM/DSS model mice. Additionally, we demonstrated that the 3'untranslated region (UTR) of AKT2 was a direct target of miRNA-200b through bioinformatics analysis and dual-luciferase assay. Collectively, these findings suggest that miRNA-200b's contribution to tumor-suppressing program was correlated with EMT and inflammatory responses in a AKT2-dependent manner.