14 research outputs found

    Joining S100 proteins and migration:for better or for worse, in sickness and in health

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    The vast diversity of S100 proteins has demonstrated a multitude of biological correlations with cell growth, cell differentiation and cell survival in numerous physiological and pathological conditions in all cells of the body. This review summarises some of the reported regulatory functions of S100 proteins (namely S100A1, S100A2, S100A4, S100A6, S100A7, S100A8/S100A9, S100A10, S100A11, S100A12, S100B and S100P) on cellular migration and invasion, established in both culture and animal model systems and the possible mechanisms that have been proposed to be responsible. These mechanisms involve intracellular events and components of the cytoskeletal organisation (actin/myosin filaments, intermediate filaments and microtubules) as well as extracellular signalling at different cell surface receptors (RAGE and integrins). Finally, we shall attempt to demonstrate how aberrant expression of the S100 proteins may lead to pathological events and human disorders and furthermore provide a rationale to possibly explain why the expression of some of the S100 proteins (mainly S100A4 and S100P) has led to conflicting results on motility, depending on the cells used. © 2013 Springer Basel

    Annexin II tetramer: structure and function

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    Pathologies Involving the S100 Proteins and Rage

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    Annexin II: Analysis of a Pleiotropic Protein

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    Assays for Insulin and Insulin-Like Signal Transduction Based on Adipocytes, Hepatocytes, and Myocytes

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    After having established insulin-like activity of compounds/drug candidates in primary or cultured adipose, muscle, and liver cells or tissues with one or several of the metabolic assays described above (see K.6.1 and K.6.2), it is often useful to elucidate the molecular mode of action of these compounds/drug candidates for further characterization and optimization, in particular regarding selectivity and potency. For this, detailed knowledge in the molecular mechanisms of the insulin signal transduction cascade as well as of cross-talking insulin-like signaling pathways as well as the availability of appropriate reliable and robust cell-free and cell-based assays reflecting these events is required. The following view results from the current experimental findings but, due to limitations in space and rapid progress still made in this area, has to be considered as simplified and temporary, only
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