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Tat D11—Novus高效诱导自噬新武器

Tat D11—Novus高效诱导自噬新武器

Tat D11—Novus高效诱导自噬新武器


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。

Beclin-1是自噬的关键正调控因子


产品列表:


目录号

产品名称

规格

LB-56888

Tat-Beclin 1 D11 Autophagy Inducing Peptide

1mg

LB-56886

Tat-Beclin 1 L11 Autophagy Inducing Peptide

1mg

LB-56887

Tat-Beclin 1 L11S Autophagy Inducing Peptide

1mg



Tat-D11 and Tat-L11 are more potent autophagy inducersthan Tat-Beclin 1. HeLa GFP-LC3B were treated with Tat-D11, Tat-L11, Tat-L11Sor Tat-Beclin for 1.5 hrs, and (A) the number of autophagosomes were assessedby fluorescent microscopy and (B) the number of GFP+/ LC3B+ spots werequantified


Figure 1. Tat-D11 and Tat-L11 are more potent autophagy inducersthan Tat-Beclin 1. HeLa GFP-LC3B were treated with Tat-D11, Tat-L11, Tat-L11Sor Tat-Beclin for 1.5 hrs, and (A) the number of autophagosomes were assessedby fluorescent microscopy and (B) the number of GFP+/ LC3B+ spots werequantified


Dose-response induction of GFP-LC3B in Hela cellsby Tat-D11. Inset figure shows that the Tat-D11 is a more potent inducer ofautophagy than the Tat-Beclin-1 peptide.


Figure 2. Dose-response induction of GFP-LC3B in Hela cellsby Tat-D11. Inset figure shows that the Tat-D11 is a more potent inducer ofautophagy than the Tat-Beclin-1 peptide.


Induction of LC3B and downregulation of p62 in Helacells by Tat-D11 and Tat-L11.


Figure 3 Induction of LC3B and downregulation of p62 in Helacells by Tat-D11 and Tat-L11.

参考文献:

1. Mizushima, N. and D.J.Klionsky, Protein turnover via autophagy: implications for metabolism. Annu RevNutr, 2007. 27: p. 19-40.

2. Stolz, A., A. Ernst, and I.Dikic, Cargo recognition and trafficking in selective autophagy. Nat Cell Biol,2014. 16(6): p. 495-501.

3. Kuma, A., et al., The role ofautophagy during the early neonatal starvation period. Nature, 2004. 432(7020):p. 1032-6.

4. Komatsu, M., et al., Loss ofautophagy in the central nervous system causes neurodegeneration in mice.Nature, 2006. 441(7095):p.880-4.

5. Hara, T., et al., Suppressionof basal autophagy in neural cells causes neurodegenerative disease in mice.Nature, 2006.441(7095): p. 885-9.

6. Nakai, A., et al., The roleof autophagy in cardiomyocytes in the basal state and in response tohemodynamic stress. Nat Med, 2007. 13(5): p.619-24.

7. Masiero, E., et al.,Autophagy is required to maintain muscle mass.Cell Metab, 2009. 10(6): p.507-15.

8. Glick, D., S. Barth, and K.F.Macleod, Autophagy: cellular and molecular mechanisms. J Pathol, 2010. 221(1):p. 3-12.

9. Shoji-Kawata, S., et al.,Identification of a candidate therapeutic autophagy-inducing peptide. Nature,2013. 494(7436): p. 201-6.

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