A viral infection-biomimetic strategy for antibody-guided targeted protein degradation
Source abstract
Abstract
Targeted protein degradation (TPD) is a valuable strategy for investigating protein functionality in cell biology and drug discovery. Among the various emerging TPD technologies, antibody-guided TPD offers key advantages over other protein degradation methods in terms of compatibility with different proteins of interest (POIs) and cell types. However, increasing the efficiency of cellular antibody internalisation and protein degradation remains challenges. Inspired by viral infection, which often efficiently activates protein degradation pathways in host cells, we developed a strategy called virus infection-mimicking targeted protein degradation (ViTPD) as a universal platform for degrading intracellular proteins. By mimicking three features of viral infection, we produced ViTPD nanoparticles by biomineralising antibodies enveloped by viral membranes or mixed with IFN-α. The biomineralised shell enhanced the cellular uptake of ViTPD nanoparticles via clathrin-mediated endocytosis. Similar to viral neutralising antibodies entering cells, the Fab region of the antibody released from ViTPD nanoparticles binds the POI, while the Fc region can recruit TRIM21, a key enzyme that continuously consumes during protein degradation. Interestingly, viral membrane components or IFN-α in the ViTPD led to increased TRIM21 expression, which enhanced the efficiency of proteolysis. ViTPD can effectively degrade several POIs, including GFP, FAK, COPZ1 and TREX1. Collectively, our results demonstrate that ViTPD provides a novel design strategy and an efficient nanoplatform for targeting intracellular protein degradation. STATEMENT OF SIGNIFICANCE: Antibody-guided targeted protein degradation (TPD) exhibits superior versatility compared to conventional degradation methods, demonstrating broad compatibility with diverse proteins of interest (POIs) across various cell types. Despite these advantages, significant challenges persist in optimizing cellular antibody internalization efficiency and degradation kinetics. In this study, we developed ViTPD, a biomimetic TPD platform that mimicking three viral infection features: (1) virus-like cellular internalization pathways, (2) virus-neutralizing antibody behavior, and (3) host-mediated protein degradation responses during viral infection. The development of ViTPD provides not only a robust platform for degrading diverse intracellular POIs but also establishes new design principles for next-generation protein degradation systems. This platform establishes new design principles for next-generation TPD systems while expanding therapeutic potential for precision medicine.
Source: europepmc · Quality: candidate unverified · Source record ↗
Research context
OpenAlex topics: Protein Degradation and Inhibitors · CAR-T cell therapy research · Virus-based gene therapy research
SciVX discovery tags are terminology-based. OpenAlex topics are source-provided classifications.
References (46)
Show source-provided references
1. Protacs: chimeric molecules that target proteins to the Skp1-Cullin-F box complex for ubiquitination and degradation10.1073/pnas.141230798 ↗
2. PROTAC targeted protein degraders: the past is prologue10.1038/s41573-021-00371-6 ↗
3. The AUTOTAC chemical biology platform for targeted protein degradation via the autophagy-lysosome system10.1038/s41467-022-28520-4 ↗
4. LYTACs that engage the asialoglycoprotein receptor for targeted protein degradation10.1038/s41589-021-00770-1 ↗
5. Development of antibody-based PROTACs for the degradation of the cell-surface immune checkpoint protein PD-L110.1021/jacs.0c10008 ↗
6. Covalently engineered nanobody chimeras for targeted membrane protein degradation10.1021/jacs.1c08521 ↗
7. Acute and rapid degradation of endogenous proteins by Trim-away10.1038/s41596-018-0028-3 ↗
8. A method for the acute and rapid degradation of endogenous proteins10.1016/j.cell.2017.10.033 ↗
9. Degrader-antibody conjugates10.1039/D2CS00141A ↗
10. Antibody conjugation of a chimeric BET degrader enables in vivo activity10.1002/cmdc.201900497 ↗
11. Emerging new therapeutic antibody derivatives for cancer treatment10.1038/s41392-021-00868-x ↗
12. Promises and pitfalls of intracellular delivery of proteins10.1021/bc500320j ↗
13. Controlled release of therapeutic antibody formats10.1016/j.ejpb.2014.08.001 ↗
14. Antibody drug conjugate: the "biological missile" for targeted cancer therapy10.1038/s41392-022-00947-7 ↗
15. Autophagy during viral infection - a double-edged sword10.1038/s41579-018-0003-6 ↗
16. Translation-a tug of war during viral infection10.1016/j.molcel.2022.10.012 ↗
17. Stress responses to viral infection10.1016/0966-842X(94)90540-1 ↗
18. Antiviral neutralizing antibodies: from in vitro to in vivo activity10.1038/s41577-023-00858-w ↗
19. Beyond binding: antibody effector functions in infectious diseases10.1038/nri.2017.106 ↗
20. Type I interferon/STAT1 signaling regulates UBE2M-mediated antiviral innate immunity in a negative feedback manner10.1016/j.celrep.2023.112002 ↗
21. TRIM21: a cytosolic fc receptor with broad antibody isotype specificity10.1111/imr.12363 ↗
22. Mineralized state of the avian influenza virus in the environment10.1002/anie.201705769 ↗
23. Calcification of cell membranes: from ions to minerals10.1016/j.chemgeo.2022.121266 ↗
24. Bio-precipitation of calcium and magnesium ions through extracellular and intracellular process induced by Bacillus licheniformis SRB210.3390/min9090526 ↗
25. Nanomodification of living organisms by biomimetic mineralization10.1007/s12274-014-0509-9 ↗
26. Improvement of organisms by biomimetic mineralization: a material incorporation strategy for biological modification
27. Endosomal escape pathways for delivery of biologicals10.1016/j.jconrel.2010.11.004 ↗
28. A versatile pH-responsive platform for intracellular protein delivery using calcium phosphate nanoparticles10.1039/C5TB01760B ↗
29. Development of a virus-mimicking nanocarrier for drug delivery systems: the bio-nanocapsule10.1016/j.addr.2015.10.003 ↗
30. Overcoming biological barriers by virus-like drug particles for drug delivery10.1016/j.addr.2023.115134 ↗
31. The Hsp70 chaperone network10.1038/s41580-019-0133-3 ↗
32. Hsp70 acts as a fine-switch that controls E3 ligase CHIP-mediated TAp63 and DeltaNp63 ubiquitination and degradation10.1093/nar/gkab081 ↗
33. Role of reactive oxygen species in age-related neuromuscular deficits10.1113/JP270564 ↗
34. The dynamics of mitochondrial DNA heteroplasmy: implications for human health and disease10.1038/nrg3966 ↗
35. Oxidative stress: roles in skeletal muscle atrophy10.1016/j.bcp.2023.115664 ↗
36. A comprehensive mathematical model for three-body binding equilibria10.1021/ja311795d ↗
37. Intracellular antibody-bound pathogens stimulate immune signaling via the Fc receptor TRIM2110.1038/ni.2548 ↗
38. TRIM Family proteins: roles in autophagy, immunity, and carcinogenesis10.1016/j.tibs.2017.01.002 ↗
39. The RING finger protein family in health and disease10.1038/s41392-022-01152-2 ↗
40. TRIMs: selective recruitment at different steps of the NF-kappaB pathway-determinant of activation or resolution of inflammation10.1007/s00018-021-03900-z ↗
41. TRIM27 interacts with Ikappabalpha to promote the growth of human renal cancer cells through regulating the NF-kappaB pathway10.1186/s12885-021-08562-5 ↗
42. UBE2L3, a partner of MuRF1/TRIM63, is involved in the degradation of myofibrillar actin and myosin10.3390/cells10081974 ↗
43. A muscle-specific MuRF1-E2 network requires stabilization of MuRF1-E2 complexes by telethonin, a newly identified substrate10.1002/jcsm.12249 ↗
44. Translocalized IgA mediates neutralization and stimulates innate immunity inside infected cells10.1073/pnas.1410980111 ↗
45. Biomineralization: from material tactics to biological strategy10.1002/adma.201605903 ↗
46. Guidelines derived from biomineralized tissues for design and construction of high-performance biomimetic materials: from weak to strong10.1039/D2CS00513A ↗