自噬就是細胞水平上的一種“自殘”，依賴于溶酶體降解掉自身的一些細胞質元件，細胞利用這一過程在饑餓情況下快速回收細胞物質或清除受損的細胞器和有害蛋白，自噬也是介導先天免疫反應，清除病毒和其他細胞內微生物的一種特別途徑。
Beclin-1是自噬的關鍵正調控因子，是自噬體形成的必要條件，Novus的Tat-D11將Beclin-1上發揮重要作用的11個氨基酸與一種細胞滲透性肽相融合，有效誘導細胞自噬。原理如下圖所示，GAPR-1與Beclin-1結合后抑制自噬形成，而Tat-D11的存在能夠讓Beclin-1解離下來，從而誘導自噬形成。
產品列表：
| 目錄號 | 產品名稱 | 規格 |
| 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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