Tat-Beclin 1 D11 Autophagy Inducing Peptide - Retroinverso form

Immunocytochemistry/Immunofluorescence: Tat-Beclin 1 D11 Autophagy Inducing Peptide [NBP2-49888] - HeLa GFP-LC3B cells were treated with Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S for 1.5 hours. Thereafter, the cells were stained using NeuroTrace Red or DAPI and analyzed employing fluorescent microscopy. Note the higher number of autophagosomes/GFP-LC3B+ puncta in the images of Tat-D11 and Tat-L11 treated cells when compared to Tat-Beclin 1 and Tat-L11S treated cells.

In vitro assay: Tat-Beclin 1 D11 Autophagy Inducing Peptide - Retroinverso form [NBP2-49888] - Analysis of lysates from HeLa cells that were left untreated (blank) or were treated with 10-20 uM each of Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S. The lysates were analyzed for the expression of LC3-1/LC3-II and SQSTM1/p62 using 2 ug/mL each of anti-LC3B (NB100-2220) and anti-SQSTM1/p62 (MAB8028) respectively. Anti-Actin (AF4000) was used as a loading control. TatD11 exhibited superior induction of LC3-II and down-regulation of p62 protein when compared to other treatment and control groups.

In vivo assay: Tat-Beclin 1 D11 Autophagy Inducing Peptide - Retroinverso form [NBP2-49888] - In vivo dose study in 10wk old C57BL/6J mice. Either 1mg/kg or 10mg/kg IP once daily was administered for 2 days, mice were sacrificed, kidneys prepared for Western blot analysis. Lysosomal inhibitor bafilomycin A1 was used to provide a measurement of autophagic flux. *vehicle is scrambled tat-beclin (NBP2-49887-5mg). Image from verified customer review.

• Reactivity: All-NA
• Applications: Func
• Concentration: LYOPH

Tat-Beclin 1 D11 Autophagy Inducing Peptide - Retroinverso form Summary

• Description: Tat-D11 [NBP2-49888]: peptides comprising 11 amino acids derived from Beclin 1 linked to the HIV Tat protein with a diglycine linker. These peptides are in the retero-inverso D-configuration. The amino acid sequence of Tat-Beclin 1 D11 is RRRQRRKKRGYGGDHWIHFTANWV (Bio-Techne's exclusive patent license: US Patent 8,802,633).
• Background: 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 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. 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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• Protein/Peptide Type: Autophagy Inducing Peptide

Applications/Dilutions

• Dilutions:
  • Functional
  • In vitro assay
  • In vivo assay
• Theoretical MW: 3.08 kDa.
  Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.

Packaging, Storage & Formulations

• Storage: Store at -20C in powder form. Store at -80C once reconstituted.
• Buffer: This product is supplied lyophilized. Purity is >= to 97% (HPLC)
• Concentration: LYOPH
• Reconstitution Instructions: Reconstitute with DMSO or water to desired concetration. Note:- D11 should NOT be reconstituted at a concentration greater than 5 mM.

Notes

Note: Tat-L11 and Tat-D11, are exclusively available from Novus Biologicals (Bio-Techne's exclusive patent license: US Patent 8,802,633).

Alternate Names for Tat-Beclin 1 D11 Autophagy Inducing Peptide - Retroinverso form

• Autophagy Inducing peptide
• Tat-Beclin 1 peptide
• Tat-Beclin 1
• Tat-Beclin peptide
• Tat-Beclin
• Tat-D11

Background

Many standard methods to induce autophagy lack desired specificity. Both starvation and rapamycin, an allosteric inhibitor of MTORC1, are known to regulate biological processes other than autophagy. The non-specific nature of these methods complicates data interpretation and has driven the preference for loss-of-function Atg mutants to analyze autophagy. In 2013, the discovery of engineered Tat-Beclin 1 provided the first method to induce autophagy without regulating other pathways non-specifically. Peptides composed of the autophagy-inducing region of Beclin 1 fused to the HIV-Tat protein were demonstrated to increase autophagosome and autolysosome numbers, as well as protein degradation. Since then, Tat-Beclin 1 peptides have been widely used to successfully induce autophagy both in vitro and in vivo. The peptides below are of a shorter Tat-Beclin 1 peptide with an enhanced potency to induce autophagy. This shorter peptide, Tat-D11, increases autophagosome and autolysosome induction by over fivefold compared to the longer peptide, Tat-Beclin 1. Results have demonstrated the superior potency of Tat-D11 over Tat-Beclin 1.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. This product is guaranteed for 1 year from date of receipt.

Publications for Tat-Beclin 1 Autophagy Inducing Peptide (NBP2-49888)(23)

Publications using NBP2-49888

• Vega-Rubin-de-Celis, S;Kristani, A;Kudla, M;Mergener, S;Corrochano-Ruiz, A;Larafa, S;Montero-Vergara, J;Ahle, LM;Will, R;Lever, M;Grünwald, V;Hadaschik, B;Jendrossek, V;Bechrakis, NE;Peña-Llopis, S; Autophagy suppression via SRC induction represents a therapeutic vulnerability for BAP1-mutant cancers Autophagy 2025-08-03 [PMID: 40754831]
• Yamada K, Ito M, Nunomura H et al. Rubicon, a Key Molecule for Oxidative Stress-Mediated DNA Damage, in Ovarian Granulosa Cells. Antioxidants (Basel, Switzerland) 2025-04-15 [PMID: 40298803]
• Khang Nguyen, Jialing Tang, Sungji Cho, Fan Ying, Hye Kyoung Sung, James Wonsuk Jahng, Kostas Pantopoulos, Gary Sweeney Salubrinal promotes phospho-eIF2 alpha -dependent activation of UPR leading to autophagy-mediated attenuation of iron-induced insulin resistance Molecular Metabolism 2024-03-26 [PMID: 38527647]
• Atsushi F, Tomoko S, Mihoko Y et al. Chloroquine is a safe autophagy inhibitor for sustaining the expression of antioxidant enzymes in trophoblasts Journal of Reproductive Immunology 2022-11-01 [PMID: 36470134]
• Zheng N, Fang J, Xue G et al. Induction of tumor cell autosis by myxoma virus-infected CAR-T and TCR-T cells to overcome primary and acquired resistance Cancer cell 2022-08-15 [PMID: 36027915]
• Luis LB, Ana GT, Carlos GE et al. Salmonella Promotes Its Own Survival in B Cells by Inhibiting Autophagy Cells 2022-06-29 [PMID: 35805144] (In vitro)
• Forte M, Bianchi F, Cotugno M Et al. An interplay between UCP2 and ROS protects cells from high-salt-induced injury through autophagy stimulation Cell death & disease 2021-10-08 [PMID: 34625529] (In vitro)
• Pavel M, Park SJ, Frake RA et al. alpha-Catenin levels determine direction of YAP/TAZ response to autophagy perturbation Nature communications 2021-03-17 [PMID: 33731717]
• Ramesh B. Kasetti, Prabhavathi Maddineni, Charles Kiehlbauch, Shruti Patil, Charles C. Searby, Beth Levine, Val C. Sheffield, Gulab S. Zode Autophagy stimulation reduces ocular hypertension in a murine glaucoma model via autophagic degradation of mutant myocilin JCI Insight 2021-03-08 [PMID: 33539326] (In vivo assay)
• Yang J, Kitami M, Pan H, et al. Augmented BMP signaling commits cranial neural crest cells to a chondrogenic fate by suppressing autophagic beta-catenin degradation Science signaling 2021-01-12 [PMID: 33436499]
• Soria L, Perocheau D, De Sabbata G et al. Beclin-1-mediated activation of autophagy improves proximal and distal urea cycle disorders EMBO Mol Med 2020-12-28 [PMID: 33369168]
• Mathew B, Chennakesavalu M, Sharma M et al. Autophagy and post-ischemic conditioning in retinal ischemia Autophagy 2020-05-26 [PMID: 32452260] (In vitro, Rat)
• Iaconis D, Crina C, Brillante S et al. The HOPS Complex Subunit VPS39 controls ciliogenesis through autophagy Hum. Mol. Genet. 2020-02-20 [PMID: 32077937] (Human)
• Forte M, Bianchi F, Cotugno M et al. Pharmacological restoration of autophagy reduces hypertension-related stroke occurrence Autophagy. 2019-11-12 [PMID: 31679456]
• Watanabe R, Sasaki S, Kimura N Activation of autophagy in early neonatal mice increases primordial follicle number and improves lifelong fertility Biol. Reprod. 2019-09-30 [PMID: 31566206]
• Wong M, Ganapathy AS, Suchanec E et al. Intestinal Epithelial Tight Junction Barrier regulation by Autophagy related protein ATG6/beclin 1 Am. J. Physiol., Cell Physiol. 2019-03-20 [PMID: 30892937] (Func)
• Sharif T, Martell E, Dai C et al. HDAC6 differentially regulates autophagy in stem-like versus differentiated cancer cells. Autophagy. 2018-11-16 [PMID: 30444165]
• Vega-Rubin-de-Celis S, Zou Z, Fernandez AF et al. Increased autophagy blocks HER2-mediated breast tumorigenesis Proc Natl Acad Sci U S A 2019-04-17 [PMID: 29610308] (In Vivo, Human)
• Bartolomeo R, Cinque L, De Leonibus C mTORC1 hyperactivation arrests bone growth in lysosomal storage disorders by suppressing autophagy. J Clin Invest. 2017-10-02 [PMID: 28872463] (In Vivo, Mouse)
• Peraro L, Zou Z, Makwana KM et al. Diversity-Oriented Stapling Yields Intrinsically Cell-Penetrant Inducers of Autophagy J Am Chem Soc. 2017-06-14 [PMID: 28414223] (In Vivo, Human)
• Franco LH, Nair VR, Scharn CR et al. The Ubiquitin Ligase Smurf1 Functions in Selective Autophagy of Mycobacterium tuberculosis and Anti-tuberculous Host Defense. Cell Host Microbe 2017-01-11 [PMID: 28017659] (In Vivo, Mouse)
• Pietrocola F, Pol J Vacchelli E et al. Caloric Restriction Mimetics Enhance Anticancer Immunosurveillance Cancer Cell. 2016-07-11 [PMID: 27411589] (In Vivo, Mouse)
• Shoji-Kawata S, Sumpter R, Leveno M et al. Identification of a candidate therapeutic autophagy-inducing peptide. Nature. 2013-02-14 [PMID: 23364696] (In Vivo)
  
  Details:
  Tat-beclin 1 (L-amino acid) / Tat-Beclin 1 L11 (NBP2-49886) and Tat–beclin 1 (D-amino acid)/Tat-Beclin 1 D11, Retroinverso form (NBP2-49888) along with the control peptide Tat-scrambled (L-amino acid)/Tat-Beclin 1 L11S Peptide, Scrambled Control (NBP2-49887) were tested in-vivo for the induction of autophagy. 6-week-old GFP-LC3 transgenic mice, and normal or CHIKV and WNV Egypt strain virus infected 5-day-old GFP-LC3 mice were injected intra-peritoneally (i.p.) with these Tat-beclin derivative peptides at a dose of 20 mg/Kg body weight (5.3uM/Kg). Brain tissues were analyzed using IHC-Frozen and Western blot analysis for measuring cell death (TUNEL Assay) and p62 expression respectively. Toxicity of these peptides was assessed in 6-day-old C57BL/6J mice via daily injections of Tat-scrambled (L-amino acid, Tat-Beclin 1 L11S) or Tat-beclin 1 (L-amino acid, Tat-Beclin 1 L11) at 15 mg kg-1 and Tat–beclin 1 (D-amino acid, Tat-Beclin 1 D11) at a dose of 20 mg/Kg body weight for 2 weeks (Figure 4).

Review for Tat-Beclin 1 Autophagy Inducing Peptide (NBP2-49888) (1)

Average Rating: 5

(Based on 1 review)

reviewed by: Verified Customer In vivo treatment + immunoblot analysis 01/07/2019

Summary

• Application: Other
• Lot: 1455072
• Comments: Increased basal expression of LC3-II on immunoblot as expected in the kidneys at a dose of 1mg/kg.Soluble in PBS.

Comments

• Comments: I used this peptide for an in vivo dose study in 10wk old C57BL/6J mice. I administered either 1mg/kg or 10mg/kg IP once daily for 2 days, sacrificed the mice, and prepared the kidneys for western blot analysis (image shown). Additionally, the lysosomal inhibitor bafilomycin A1 was used to provide a measurement of autophagic flux.
  *vehicle is scrambled tat-beclin (NBP2-49887-5mg)