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Intrinsic Apoptosis Pathway (intrinsic + apoptosi_pathway)
Selected AbstractsThe role of the intrinsic apoptosis pathway in platelet life and deathJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2009B. T. KILE Summary., In recent years, it has become increasingly apparent that the production of platelets and their subsequent life span in the circulation are regulated, at least in part, by apoptotic mechanisms. There is also evidence implicating the apoptotic machinery in the regulation of platelet functional responses. This review examines the role of the intrinsic apoptosis pathway, regulated by the Bcl-2 family of proteins, in platelet biology. [source] Immunohistochemical analysis of phospho-BAD protein and mutational analysis of BAD gene in gastric carcinomas,APMIS, Issue 8 2007EUN GOO JEONG Mounting evidence indicates that deregulation of apoptosis contributes to the development of human cancers. BAD, a proapoptotic Bcl-2 family protein, regulates the intrinsic apoptosis pathway. The aim of this study was to explore whether alterations of phospho-BAD (p-BAD) protein that antagonizes apoptosis function of BAD and mutation of BAD gene are characteristics of human gastric cancers. We analyzed expression of p-BAD in 60 gastric adenocarcinomas by immunohistochemistry. Also, we analyzed BAD gene for detection of somatic mutations by single-strand conformation polymorphism (SSCP) assay. p-BAD expression was detected well in normal gastric mucosal epithelial cells, whereas it was detected in only 51% (31 of the 60) of the cancers. There was no somatic mutation of BAD gene in the 60 gastric cancer samples. The decreased expression of p-BAD in malignant gastric epithelial cells compared to normal mucosal epithelial cells suggested that loss of p-BAD expression may play a role in gastric tumorigenesis. The data also suggest that BAD mutation may not be a direct target of inactivation in gastric tumorigenesis. [source] The effect of Bcl-2, YAMA, and XIAP over-expression on apoptosis and adenovirus production in HEK293 cell lineBIOTECHNOLOGY & BIOENGINEERING, Issue 4 2009Kalbinder Singh Sandhu Abstract Many viruses induce cell death and lysis as part of their replication and dissemination strategy, and in many cases features of apoptosis are observed. Attempts have been made to further increase productivity by prolonging cell survival via the over-expression of anti-apoptotic genes. Here, we extend the study to investigate the association between virus replication and apoptosis, pertinent to large-scale vector production for gene therapy. Infection of an HEK293 cell line with a replication defective type-5-adenovirus expressing a GFP reporter (Ad5GFP) resulted in rapid decline in viability associated with increased virus titer. The over-expression of bcl-2 resulted in improved cell resistance to apoptosis and prolonged culture duration, but reduced virus specific and total productivity. In contrast, the over-expression of pro-caspase-3 (Yama/CPP32/apopain) resulted in reduced cell survival but increased virus productivity. The treatment of infected cells with caspase inhibitors support the preposition that caspase-3 dependent apoptosis, and to a lesser degree caspase-9 dependent apoptosis, represent important steps in virus production, thus implicating the intrinsic apoptosis pathway in the production of adenovirus from HEK293 cells. The suppression of apoptosis by the over-expression of XIAP (inhibitors of caspase family cell death proteases) further shows that caspase-mediated activation plays an important role in virus infection and maturation. Biotechnol. Bioeng. 2009; 104: 752,765 © 2009 Wiley Periodicals, Inc. [source] | ||||||||||