Furthermore, to increase selective targeting of RavZ-based sensors into LC3- or GABARAP-positive autophagic membranes, we replaced the LIR motifs of RavZ with selective LC3- or GABARAP subfamily-binding LIR motifs and developed additional RavZ-based probes that were selectively detecting for LC3- or GABARAP-positive autophagic membranes in cells.

半胱氨酸蛋白酶atg4b执行两个lc3/gabarap处理事件：启动新合成的pro-lc3/gabarap以实现脂化(新翻译的lc3b，称为pro-lc3，在c-末端被半胱氨酸蛋白酶atg4b切割，得到lc3-i)和在自溶酶体中货物降解后脂化lc3/gabarap的去调节（fig.4）。

Jan 12, 2016 · ATGL exhibits LC3-interacting region (LIR) motifs, and mutating a single LIR motif on ATGL displaces ATGL from LD and disrupts lipolysis. Thus, cold-induced activation of central autophagy activates lipophagy and cytosolic lipases in a complementary manner to mediate lipolysis in peripheral tissues.

Nov 23, 2023 · WB结果证实，在海马和/或 皮 层 组 织中，GP17、RAP 和/或 3-MA 增 加 了Beclin1 和 LC3-B 的表达，抑制了 P62 的表达(图 2E-I)。 透射电镜（TEM）结果显示 MCAO/R 诱导了自噬小体的积累，而 GP-17、RAP 和 3-MA 处理促进了多个自噬空泡的形成(图2J)。

通过Western印迹定量LC3蛋白的表达和直接mTORC1靶标p70S6K1-T389的磷酸化。 使用共聚焦荧光成像，lysotracker，和活细胞成像。 RAP减少了PA诱导的细胞凋亡。

Download scientific diagram | Effects of 3-MA Rap on LC3 and active caspase 3 in H9c2 cells. H9c2 cells were treated with 3-MA for 24 h or Rap for 12 h under normal conditions and for 150 min...

因此,本研究建立脂多糖(LPS)所 致脓毒症急性肺损伤模型,分别用自噬促进剂雷帕霉素(rapamycin,RAP)和自噬抑制剂3 甲 基腺嘌呤(3 methyladenine,3 MA)干预,观 察自噬的改变和脓毒症肺损伤的关系。 1 1 试剂雷帕霉素(rapamycin,RAP,纯 度大于98%)、3 甲 基腺嘌呤(3 methyladenine,3 MA,纯 度>98%)、脂...

LC3/Atg8 被具有蛋白内切酶活性的 Atg4 在羧基端剪切，生成胞浆型 LC3-I。 在自噬形成时，胞浆型LC3-I通过 Atg7 和 Atg3 （分别对应泛素激活酶E1和泛素结合酶E2）参与的类泛素样反应，使 磷脂酰乙醇胺 (PE) 偶联，生成脂质化形式的 LC3，也称作 LC3-II，它附着到自噬体 (autophagosome)的膜上，是自噬体的结构蛋白，即自噬体膜型LC3-II。 在降解过程中，位于自噬溶酶体外膜的LC3-II被半胱氨酸蛋白酶Atg4B切割，产生LC3-I循环利用；位于内膜的LC3-II则 …

Mar 20, 2025 · A3Bp shows a much more attenuated increase in GFP-LC3 puncta formation in the presence of Rap (Figure 4 D), which highlights the importance of building block 220 (Figure 2 D) and is consistent with the screening results.

To better characterize this assay in mammalian cells, HeLa cells stably expressing GFP-LC3 were treated with rapamycin (Rap), a well-known autophagy inducer by suppressing mTOR, 26 for different concentrations and time points. Rap increased the number of GFP-LC3 puncta in a concentration-dependent manner (Fig. 1A and B).