ATG5型
自噬
ATG16L1
化学
ATG12
肽
细胞生物学
脂锚定蛋白
泛素
生物化学
细胞凋亡
基因
生物
作者
Jin Cui,Yuta Ogasawara,Ikuko Kurata,Kazuaki Matoba,Yūko Fujioka,Nobuo N. Noda,Masakatsu Shibasaki,Takumi Watanabe
摘要
Selective modulation of autophagy is a promising therapeutic strategy, especially for cancer treatment. However, the lack of specific autophagy inhibitors limits this strategy. The formation of the ATG12-ATG5-ATG16L1 complex is essential for targeting the ATG12-ATG5 conjugate to proper membranes and to generate LC3-II for the progression of autophagy. Thus, targeting ATG5-ATG16L1 protein-protein interactions (PPIs) might inhibit early stage autophagy with high specificity. In this paper, we report that a stapled peptide derived from ATG16L1 exhibits potent binding affinity to ATG5, striking resistance to proteolysis, and significant autophagy inhibition activities in cells.
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