中国病理生理杂志2011，Vol.27Issue(4)：749-754,6.DOI:10.3969/j.issn.1000-4718.2011.04.024
PI3K/Akt调控内质网应激对GRP78的诱导
PI3K/Akt regulates endoplasmic reticulum stress-mediated GRP78 induction
摘要
Abstract
AIM: To investigate the effect of PI3K/Akt pathway on endoplasmic reticulum ( ER ) stress - mediated glucose - regulated protein 78 ( GRP78 ) induction in human embryonic kidney 293 cells ( HEK293 ) cells.METHODS : PDK inhibitor LY294002, dominant negative kinase - dead mutant vector for HA - Akt ( K179M ) and Akt1 siRNAs were used to block the PI3K/Akt pathway under ER stress.Constitutively active expression vectors for Akt ( myr - HA -Akt ) were used to up - regulate Akt activity under ER stress.The effects of PI3K/Akt on ER stress - mediated GRP78 induction in HEK293 cells were determined by Western blotting and RT - PCR.RESULTS: GRP78 induction was inhibited by LY294002, Akt1 ( K179M ) and Akt1 siRNA, but was increased by myr - Akt1 in dithiothreitol - and thapsigargin -treated HEK293 cells.However, both myr - Akt2/3 and Akt2/3 siRNA had no effect on GRP78 induction in HEK293 cells under ER stress.Furthermore, the PI3K/Akt pathway didn't regulated GRP78mRNA induction but increased GRP78 protein stability.CONCLUSION: PI3K/Akt promotes GRP78 accumulation through increasing the stability of GRP78 protein in HEK293 cells under ER stress.关键词
PI3K/Akt/葡萄糖调节蛋白质78/内质网应激/HEK293细胞分类
医药卫生引用本文复制引用
刘友平,严冬梅,陈川宁,段春燕,陈绍坤,李洪,代荣阳..PI3K/Akt调控内质网应激对GRP78的诱导[J].中国病理生理杂志,2011,27(4):749-754,6.基金项目
国家自然科学基金资助项目(No.81000886) （No.81000886）
四川省教育厅科技基金资助项目(No.09ZA050) （No.09ZA050）
四川省卫生厅科技基金资助项目(No.2007-431) （No.2007-431）
