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IBJ-Iranian Biomedical Journal. 2016; 20 (1): 63-67
in English | IMEMR | ID: emr-174279

ABSTRACT

Background: Recently, it has been revealed that tyrosine kinase inhibitors [TKIs] act through inducing both oxidative and endoplasmic reticulum [ER] stress in chronic myeloid leukemia cells. However, ER stress signaling triggers both apoptotic and survival processes within cells. Nevertheless, mechanisms by which TKIs avoid the pro-survival effects are not clear. The aim of this study was to evaluate the potential role of oxidative stress in activity of unfolded protein response [UPR] survival pathway within K562 cell line


Methods: The expression of UPR survival target genes, Xbpl, and Grp94 [glucose requiring protein 94] was studied in single and combined exposure to oxidative and ER stress in K562 cell line by quantitative and qualitative PCR


Results: The expression of UPR-related survival gene Grp94 was hampered by exposing to oxidative stress in cell induced with ER stress


Conclusion: Interaction of oxidative and ER stress may role as a mediator influencing UPR signaling activity

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