自噬就是细胞水平上的一种“自残”，依赖于溶酶体降解掉自身的一些细胞质元件，细胞利用这一过程在饥饿情况下快速回收细胞物质或清除受损的细胞器和有害蛋白，自噬也是介导先天免疫反应，清除病毒和其他细胞内微生物的一种特别途径。
Beclin-1是自噬的关键正调控因子，是自噬体形成的必要条件，Novus的Tat-D11将Beclin-1上发挥重要作用的11个氨基酸与一种细胞渗透性肽相融合，有效诱导细胞自噬。原理如下图所示，GAPR-1与Beclin-1结合后抑制自噬形成，而Tat-D11的存在能够让Beclin-1解离下来，从而诱导自噬形成。
产品列表：
| 目录号 | 产品名称 | 规格 |
| H6-NBP2-49888 | Tat-Beclin 1 D11 Autophagy Inducing Peptide | 1mg |
| H6-NBP2-49886 | Tat-Beclin 1 L11 Autophagy Inducing Peptide | 1mg |
| H6-NBP2-49887 | Tat-Beclin 1 L11S Autophagy Inducing Peptide | 1mg |
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| Figure 1. Tat-D11 and Tat-L11 are more potent autophagy inducers than Tat-Beclin 1. HeLa GFP-LC3B were treated with Tat-D11, Tat-L11, Tat-L11S or Tat-Beclin for 1.5 hrs, and (A) the number of autophagosomes were assessed by fluorescent microscopy and (B) the number of GFP+/ LC3B+ spots were quantified |
| Figure 2. Dose-response induction of GFP-LC3B in Hela cells by Tat-D11. Inset figure shows that the Tat-D11 is a more potent inducer of autophagy than the Tat-Beclin-1 peptide. |  |
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Figure 3 Induction of LC3B and downregulation of p62 in Hela cells by Tat-D11 and Tat-L11. |
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