tailieunhanh - Báo cáo sinh học: " The involvement of survival signaling pathways in rubella-virus induced apoptosis"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: The involvement of survival signaling pathways in rubella-virus induced apoptosis | Virology Journal BioMed Central Research Open Access The involvement of survival signaling pathways in rubella-virus induced apoptosis Samantha Cooray 1 2 3 Li Jin1 and Jennifer M Best2 Address 1Enteric Neurological and Respiratory Virus Laboratory Health Protection Agency 61 Colindale Avenue London NW9 5HT UK 2Department of Infectious Diseases Virology Section Guy s King s and St. Thomas School of Medicine St. Thomas Hospital London SE1 7EH UK and 3Present address Department of Virology 3rd Floor Wright Flemming Institute Imperial College Faculty of Medicine Norfolk Place London W2 1PG UK Email Samantha Cooray - Li Jin - Jennifer M Best - Corresponding author Published 04 January 2005 Received 22 November 2004 Accepted 04 January 2005 Virology Journal 2005 2 1 doi 1743-422X-2-1 This article is available from http content 2 1 1 2005 Cooray et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Rubella virus RV causes severe congenital defects when acquired during the first trimester of pregnancy. RV cytopathic effect has been shown to be due to caspase-dependent apoptosis in a number of susceptible cell lines and it has been suggested that this apoptotic induction could be a causal factor in the development of such defects. Often the outcome of apoptotic stimuli is dependent on apoptotic proliferative and survival signaling mechanisms in the cell. Therefore we investigated the role of phosphoinositide 3-kinase PI3K -Akt survival signaling and Ras-Raf-MEK-ERK proliferative signaling during RV-induced apoptosis in RKI3 cells. Increasing levels of phosphorylated ERK Akt and GSK3P were detected from 24-96 hours post-infection .