Identification of a candidate therapeutic autophagy-inducing peptide
Open accessAbstract
The lysosomal degradation pathway of autophagy has a crucial role in defence against infection, neurodegenerative disorders, cancer and ageing. Accordingly, agents that induce autophagy may have broad therapeutic applications. One approach to developing such agents is to exploit autophagy manipulation strategies used by microbial virulence factors. Here we show that a peptide, Tat-beclin 1-derived from a region of the autophagy protein, beclin 1, which binds human immunodeficiency virus (HIV)-1 Nef-is a potent inducer of autophagy, and interacts with a newly identified negative regulator of autophagy, GAPR-1 (also called 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 or West Nile virus. Thus, through the characterization of a domain of beclin 1 that interacts with HIV-1 Nef, we have developed an autophagy-inducing peptide that has potential efficacy in the treatment of human diseases.
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MTOR-independent methods for stimulating autophagy include direct stimulation of AKT and BECN1, activating MAPK8/JNK1 to dissociate BCL2 from BECN1, applying Tat-Beclin 1, SIRT1-associated starvation, and disrupting nonsense-mediated RNA decay.
“The array of MTOR-independent methods for stimulating autophagy also includes direct stimulation of AKT and BECN1, activating MAPK8/JNK1 to dissociate BCL2 from (and thereby disinhibit) BECN1, applying the synthetic peptide Tat-Beclin 1, SIRT1-associated starvation, and disrupting nonsense-mediated RNA decay [513–517] (Figure 3).”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [516]
mTOR-independent autophagy-inducing agents include activators of AMPK and SIRT1, chemicals that reduce intracellular inositol or IP3 levels (lithium, carbamazepine, sodium valproate), K+-ATP channel opener minoxidil and Tat-beclin 1 peptide.
“mTOR-independent autophagy-inducing agents include activators of AMPK29 and SIRT136, chemicals that reduce intracellular inositol or IP3 levels (such as lithium, carbamazepine and sodium valproate), the K+-ATP channel opener minoxidil and the Tat–beclin 1 peptide, among others193-195.”
From Autophagy in kidney homeostasis and disease (2020) · cites this paper as [194]
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Protein Misfolding and Aggregation as a Therapeutic Target for Polyglutamine Diseases
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Targeting the Autophagy/Lysosomal Degradation Pathway in Parkinsons Disease
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Comprehensive autophagy evaluation in cardiac disease models
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Enhancement of hepatic autophagy increases ureagenesis and protects against hyperammonemia
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- Authors
- Shoji-Kawata, S., Sumpter, R., Leveno, M., Campbell, G. R., Zou, Z., Kinch, L., Wilkins, A. D., Sun, Q., Pallauf, K., MacDuff, D., Huerta, C., Virgin, H. W., Helms, J. B., Eerland, R., Tooze, S. A., Xavier, R., Lenschow, D. J., Yamamoto, A., King, D., Lichtarge, O., Grishin, N. V., Spector, S. A., Kaloyanova, D. V., & Levine, B.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- University of California San Diego (US)
- Howard Hughes Medical Institute (US)
- Baylor College of Medicine (US)
- Washington University in St. Louis (US)
- Utrecht University (NL)
- Cancer Research UK (GB)
- Broad Institute (US)
- Columbia University (US)
- Corresponding author
- Levine, Beth
- ORCID
- Venue
- Nature
- Published
- 2013-01-30
- Volume
- 494
- Issue
- 7436
- Pages
- 201-206
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3788641
- OpenAlex
- W2161594732
- Cited by
- 760
- References
- 48
- Citations by year
- 2026: 20 · 2025: 36 · 2024: 47 · 2023: 36 · 2022: 55 · 2021: 67 · 2020: 80 · 2019: 65 · 2018: 54 · 2017: 67 · 2016: 64 · 2015: 65 · 2014: 58 · 2013: 45
- FWCI
- 55.81
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Utrecht University Repository (Utrecht University) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Cancer Research UK (15153)
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (817.02.023)
- National Cancer Institute (P30CA142543)
- National Institute of General Medical Sciences (R01GM094575, T32GM008297, R01GM066099, R0I GM079656, R01GM079656, R0I GM066099)
- National Institute of Allergy and Infectious Diseases (K08AI099150, U54AI057160, U54AI057156)
- National Institute of Diabetes and Digestive and Kidney Diseases (R0I DK086502, R01DK083756, RC1DK086502, R0I DK083756)
- National Institute of Neurological Disorders and Stroke (R01NS084912, R0I NS063973, R01NS050199, R01NS077111, R0I NS077874, R01NS077874, R01NS063973)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- autophagy induction, Beclin-1, cell-permeable peptide, HIV-1 Nef, viral clearance, chikungunya virus, West Nile virus, lysosomal degradation, antiviral therapy
- MeSH terms
- Beclin-1, Amino Acid Sequence, Animals, Autophagy, Cell Membrane Permeability, Cells, Cultured, Chikungunya virus, HeLa Cells, Humans, Macrophages, Membrane Proteins, Molecular Sequence Data, Peptide Fragments, Recombinant Fusion Proteins, Virus Replication, West Nile virus, HIV-1, Apoptosis Regulatory Proteins, Mice, nef Gene Products, Human Immunodeficiency Virus, tat Gene Products, Human Immunodeficiency Virus
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