CAJ | 학술논문

肿瘤细胞的内质网应激非常普遍,内质网内大量未折叠或错误折叠的蛋白质蓄积可诱发未折叠蛋白反应(UPR).研究表明,初期UPR可保护细胞,恢复内质网功能和内环境稳态,后期则促进细胞凋亡.TRIB3是哺乳动物假性蛋白激酶家族Tribbles中的一员,其在UPR中起重要的枢纽作用,既能促进肿瘤细胞凋亡又可起保护作用.
종류세포적내질망응격비상보편,내질망내대량미절첩혹착오절첩적단백질축적가유발미절첩단백반응(UPR).연구표명,초기UPR가보호세포,회복내질망공능화내배경은태,후기칙촉진세포조망.TRIB3시포유동물가성단백격매가족Tribbles중적일원,기재UPR중기중요적추뉴작용,기능촉진종류세포조망우가기보호작용.
Endoplasmic reticulum stress in tumor cells is common,the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum can lead to unfolded protein response (UPR).Research shows that UPR can protect cells,reestablish endoplasmic reticulum function and homeostasis at initial stage,and can promote apoptotic at later stage.TRIB3 is one of the mammal pseudoprotein kinase family Tribbles,and plays an important pivotal role in UPR,which can not only promote apoptosis but also play a protective role.