In addition, this organism also possesses all the principal signaling cascades that modulate the cell metabolism in response to nutrient availability in higher eukaryotes, including the TOR and the PKA pathways. Therefore, yeast is an ideal system to study the regulation of autophagy by these signaling pathways. Here, we review the current state of our knowledge about the molecular events leading to the induction or inhibition of autophagy in yeast with special emphasis on the regulation of the function of Atg proteins. (C) 2009 Elsevier B.V. All rights reserved.”
“Protein

phosphatase 2B (PP2B) is one of the major brain phosphatases and can dephosphorylate tau at several phosphorylation sites in vitro. Previous studies that GNS-1480 cell line measured PP2B activity in human brain crude extracts showed that PP2B activity was either unchanged or decreased in Alzheimer’s disease (AD) brain. These results led to the speculation Cl-amidine mw that PP2B might regulate tau phosphorylation and that a down-regulation of PP2B might contribute to abnormal hyperphosphorylation of tau. In this study, we immunoprecipitated PP2B from brains of six AD subjects and seven postmortem-and age-matched controls and then measured the phosphatase activity. We found a three-fold increase in PP2B activity in AD brain as compared with control brains. The activation was due to the partial cleavage of PP2B by calpain I that was activated in AD brain. The truncation

of PP2B appeared to alter its intracellular distribution in the brain. In human brains, PP2B activity correlated positively, rather than negatively, to the levels of tau phosphorylation at several sites that can be dephosphorylated by PP2B in vitro. Truncation of PP2B in the frontal cortex was more than in the temporal cortex, and tau phosphorylation was also more in the frontal cortex. Taken together, these results indicate

that truncation of PP2B by calpain I elevates its activity but does not counteract the abnormal hyperphosphorylation of tau in AD brain.”
“The rise in pediatric obesity since the 1970s has been well established in the United States and is becoming a major concern worldwide. ABT-263 clinical trial As a potential means to help slow the obesity epidemic, low-calorie sweeteners (LCS) have gained attention as dietary tools to assist in adherence to weight loss plans or prevention of excess weight gain. Observational studies tend to show positive correlations between LCS consumption and weight gain in children and adolescents. Although the data are intriguing, these epidemiologic studies do not establish that LCS cause weight gain, because there are likely many lifestyle and genetic differences between children and families who choose to consume LCS and those who do not. Short-term randomized controlled trials have shown LCS use to be BMI neutral or to have modest weight-reducing effects in overweight and obese adolescents.