Western Blot: Tat-Beclin 1 L11S Autophagy Inducing Peptide - Inactive Form [NBP2-49887] - WB analysis of lysates from HeLa cells that were left untreated (blank) or were treated with 10-20 uM each of Tat-D11, Tat-L11, ...read more
Immunocytochemistry/ Immunofluorescence: Tat-Beclin 1 L11S Autophagy Inducing Peptide - Inactive Form [NBP2-49887] - HeLa GFP-LC3B cells were treated with Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S for 1.5 hours. ...read more
In vivo assay: Tat-Beclin 1 L11S Peptide - Scrambled Control [NBP2-49887] - In vivo dose study in mouse kidneys as control for tat-beclin D11 autophagy inducing peptide. Well tolerated by mice at dose of 1mg/kg for 2 ...read more
Tat-Beclin 1 L11S Peptide - Scrambled Control Summary
Tat-L11S [NBP2-49887]: inactive/scrambled control peptides derived from Tat-L11. These peptides are recommended as a negative control. The exact sequence of Tat-Beclin 1 L11S is YGRKKRRQRRRGGNWAWHDFVHIT (Bio-Techne's exclusive patent license: US Patent 8,802,633)
Cell-penetrating autophagy inducing peptides engineered in 2013 were demonstrated to induce autophagy through interaction with the autophagy suppressor GAPR-1/GLIPR2 (Nature, 2013; PMID 23364696). These Tat-Beclin 1 peptides were comprised of AA 267-284 of the autophagy inducer Beclin 1 (18 amino acids), a diglycine linker, and 11 amino acids of the HIV Tat protein transduction domain. Tat-B...eclin 1 peptides were re-engineered to remove 7 AA from the beclin 1 domain. These shorter peptides, Tat-D11 [NBP2-49888] and Tat-L11 [NBP2-49886], demonstrate enhanced autophagy inducing function over the original Tat-Beclin 1 peptides and the inactive/scrambled control peptide Tat-L11S [NBP2-49887]. Tat-D11 and Tat-L11 are potent autophagy inducers which function both in vitro and in vivo to specifically induce autophagy while Tat-L11S is useful as a negative control. Tat-D11 and Tat-L11 peptides are comprised of 11 amino acids of the autophagy-inducing region of beclin 1 fused to the HIV Tat protein. Both Tat-D11 and Tat-L11 peptides function by binding the negative regulator of autophagy GAPR-1/GLIPR2. Upon peptide binding, beclin 1 bound to GARP-1 is released, resulting in beclin 1 mediated autophagosome formation and autophagy induction. Data indicate Tat-D11 is more potent than both Tat-L11 and Tat-Beclin 1 in vivo. In addition, initial data derived from HeLa cells also suggests Tat-D11 is more potent than Tat-L11 in vitro. However, ongoing experiments indicate Tat-L11 may be more potent than Tat-D11 in select cell lines.
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