Tat-beclin 1, a peptide derived from a region of the autophagy protein (beclin 1), is a potent inducer of autophagy and interacts with negative regulator of autophagy, GAPR-1 (GLIPR2). Tat-beclin 1 decreases the accumulation of polyglutamine expansion protein aggregates and the replication of several pathogens (including HIV-1) in vitro, and reduces mortality in mice infected with chikungunya (CHIKV) or West Nile virus (WNV)[1].

Tat-beclin 1 (10, 30, 50 μM; 24 hours) induces autophagy and results in a dose-dependent decrease in amounts of p62, a selective autophagy substrate, and a dose-dependent conversion of the non-lipidated form of LC3, LC3-I, to the lipidated, autophagosome-associated form of LC3, LC3-II, in multiple cell lines and primary murine embryonic fibroblasts (MEFs)[1]. Tat-beclin 1 (10 μM; 2-4 hours post-infection) decreases the intracellular survival of L. monocytogenes in primary murine bone-marrow-derived macrophages (BMDMs)[1].

Tat-beclin 1 (15 mg/kg; i.p.; daily; beginning 1 day post-infection for 20 days) can induce autophagy in peripheral tissues in adult mice as well as in the central nervous system of neonatal mice (6-week-old GFP-LC3 mice)[1].

[1]. Sanae Shoji-Kawata, et al. Identification of a Candidate Therapeutic Autophagy-Inducing Peptide. Nature. 2013 Feb 14;494(7436):201-6.