Rabbit Anti-Human MAPKAPK2 (phospho Thr222) monoclonal antibody, clone U.809.5

Background: This study focuses on the identification of conserved genes involved in myocardial infarction (MI), and then analyzed the differentially expressed genes (DEGs) between the incident and recurrent events to identify MI-recurrent biomarkers. Methods: Gene expression data of MI peripheral blood were downloaded from GSE97320 and GSE66360 datasets. We identified the common DEGs in these two datasets by functional enrichment analysis and protein-protein interaction (PPI) network analysis. GSE48060 was further analyzed to validate the conserved genes in MI and to compare the DEGs between the incident and recurrent MI. Results: A total of 477 conserved genes were identified in the comparison between MI and control. Protein-protein interaction (PPI) network showed hub genes, such as MAPK14, STAT3, and MAPKAPK2. Part of those conserved genes was validated in the analysis of GSE48060. The DEGs in the incident and recurrent MI showed significant differences, including RNASE2 and A2M-AS1 as the potential biomarkers of MI recurrence. Conclusions: The conserved genes in the pathogenesis of MI were identified, benefit for target therapy. Meanwhile, some specific genes may be used as markers for the prediction of recurrent MI.

Glioblastomas are the deadliest type of brain cancer and are frequently associated with poor prognosis and a high degree of recurrence despite removal by surgical resection and treatment by chemo- and radio-therapy. Photodynamic therapy (PDT) is a treatment well known to induce mainly necrotic and apoptotic cell death in solid tumors. 5-Aminolevulinic acid (5-ALA)-based PDT was recently shown to sensitize human glioblastoma cells (LN-18) to a RIP3 (Receptor Interacting Protein 3)-dependent cell death which is counter-acted by activation of autophagy. These promising results led us to investigate the pathways involved in cell death and survival mechanisms occurring in glioblastoma following PDT. In the present study, we describe a new TSC2 (Tuberous Sclerosis 2) -dependent survival pathway implicating MK2 (MAPKAPK2) kinase and 14-3-3 proteins which conducts to the activation of a pro-survival autophagy. Moreover, we characterized a new RIP3/TSC2 complex where RIP3 is suggested to promote cell death by targeting TSC2-dependent survival pathway. These results highlight (i) a new role of TSC2 to protect glioblastoma against PDT-induced cell death and (ii) TSC2 and 14-3-3 as new RIP3 partners. (C) 2016 Published by Elsevier B.V.