Autophagy-Inducing Peptides
Tat-Beclin 1 D11 (Tat-D11) and Tat-Beclin 1 L11 (Tat-L11) peptides specifically induce autophagy and can be used both in vitro and in vivo. Tat-D11 and Tat-L11 peptides are composed of the autophagy-inducing region of Beclin 1 fused to the HIV-Tat protein to facilitate cell permeability. Both peptides demonstrate improved specificity relative to other methods of autophagy induction, as well as enhanced potency over other Beclin 1-derived autophagy inducing peptides.
Watch the video to learn more about our potent and specific Tat-D11 and Tat-L11 Autophagy-Inducing Peptides.
How They Work
Cell permeable Tat-D11 peptides compete with the autophagy inducer, Beclin 1 for binding to the negative regulator of autophagy, GAPR-1/GLIPR2. Tat-D11 peptides free Beclin-1 from GAPR-1, resulting in Beclin-1 mediated autophagy induction.
Tat-Beclin 1 D11 (Tat-D11): Peptides comprising 11 amino acids derived from the autophagy inducer Beclin 1 linked to the HIV Tat protein to increase solubility. Tat-D11 is in the D-amino acid retro-inverso configuration.
Tat-Beclin 1 L11 (Tat-L11): Peptides comprising 11 amino acids derived from the autophagy inducer Beclin 1 linked to the HIV Tat protein to increase solubility. Tat-L11 is in the naturally occurring L-configuration.
Tat-Beclin 1 L11S (Tat-L11S): An inactive, scrambled control peptide derived from Tat-L11. Tat-L11S is recommended as a negative control for Tat-D11 and Tat-L11.
Figure 1. GAPR-1/GLIPR2 is a negative regulator of autophagy and binds Beclin 1 to inhibit autophagy. In the presence of Tat-D11 peptides, Beclin 1 bound to GAPR-1 is released allowing Beclin 1 to mediate autophagosome formation and autophagy induction.
Benefits Of Tat-D11 & Tat-L11
Potency: Superior potency of Tat-D11 peptides to induce autophagy compared with other Tat-Beclin 1 peptides.
Dose: Less Tat-D11 peptide required for equal autophagy induction relative to other Tat-Beclin 1 peptides.
Specificity: Specific autophagy induction with less off-target regulation of other biological processes relative to other autophagy induction methods (e.g. rapamycin, starvation, etc)
Figure 2. Tat-D11 and Tat-L11 are specific and potent autophagy inducers. HeLa GFP-LC3B were treated with Tat-D11, Tat-L11, Tat-L11S, or Tat-Beclin 1 for 1.5 hr, and the number of GFP+/ LC3B+ spots were quantified by fluorescent microscopy.
