Anti-CTBP-2 polyclonal antibody

Oxidative stress plays a significant role in the development of hepatic insulin resistance, but the underlying molecular mechanisms remain poorly understood. In this study, we discovered that C-terminal binding protein 2 (CtBP2) level was decreased in insulin resistance. Taking into account the relationship between CtBP family protein (ANGUSTIFOLIA) and reactive oxygen species (ROS) accumulation, we conjectured CtBP2 was involved in insulin resistance through ROS induced stress. In order to verify this hypothesis, we over-expressed CtBP2 in palmitate (PA) treated HepG2 cells. Here, we found that over expression of CtBP2 ameliorated insulin sensitivity by increasing phosphorylation of glycogen synthase kinase 313 (GSK3 beta and protein kinase B (AKT). These data suggest that CtBP2 plays a critical role in the development of insulin resistance. Moreover, CtBP2 reversed the effects of PA on ROS level, lipid accumulation, hepatic glucose uptake and gluconeogenesis. We also found that over-expression of CtBP2 could suppress PA induced c-jun NH2 terminal kinase (JNK) activation. Furthermore, JNK inhibitor SP600125 was shown to promote the effect of CtBP2 on insulin signaling. Thus, we demonstrated that CtBP2 ameliorated PA-induced insulin resistance via ROS-dependent JNK pathway. (C) 2017 Elsevier Inc. All rights reserved.

We investigated DNA methylomes of pediatric B-cell acute lymphoblastic leukemias (B-ALLs) using whole-genome bisulfite sequencing and high-definition microarrays, along with RNA expression profiles. Epigenetic alteration of B-ALLs occurred in two tracks: de novo methylation of small functional compartments and demethylation of large inter-compartmental backbones. The deviations were exaggerated in lamina-associated domains, with differences corresponding to methylation clusters and/or cytogenetic groups. Our data also suggested a pivotal role of polycomb and CTBP2 in de novo methylation, which may be traced back to bivalency status of embryonic stem cells. Driven by these potent epigenetic modulations, suppression of polycomb target genes was observed along with disruption of developmental fate and cell cycle and mismatch repair pathways and altered activities of key upstream regulators.