Author: Li, Li; Wang, Li; Xiao, Ruijing; Zhu, Guoguo; Li, Yan; Liu, Changxuan; Yang, Ru; Tang, Zhiqing; Li, Jie; Huang, Wei; Chen, Lang; Zheng, Xiaoling; He, Yuling; Tan, Jinquan
Title: The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells Document date: 2011_11_21
ID: r4c1sngt_63
Snippet: Recent evidence has shown that TLR7 functions as a PRR (pattern-recognition receptor), initiating effective and appropriate antiviral responses [38] . As an ssRNA, TMV-RNA may be recognized by TLR7. Recent evidence has suggested that certain TLR signalling adaptor molecules may directly interact with components of the autophagic machinery [39] . For example, MyD88 and Trif, two signalling adaptors for TLRs, interact with the autophagy protein, Be.....
Document: Recent evidence has shown that TLR7 functions as a PRR (pattern-recognition receptor), initiating effective and appropriate antiviral responses [38] . As an ssRNA, TMV-RNA may be recognized by TLR7. Recent evidence has suggested that certain TLR signalling adaptor molecules may directly interact with components of the autophagic machinery [39] . For example, MyD88 and Trif, two signalling adaptors for TLRs, interact with the autophagy protein, Beclin1, in a manner that is enhanced by TLR signalling, and shRNA (small-hairpin RNA) knockdown of MyD88, Trif or Beclin1 inhibits TLR-induced autophagy. Here, we detected the marked accumulation of Beclin1 in HeLa cells, and we also identified the key role of Beclin1 in cellular autophagy; however, whether Beclin1 also associates with TLR signalling adaptor molecules, (thereby further mediating autophagy) was not investigated.
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