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. 2022 Dec 6;23(23):15440. doi: 10.3390/ijms232315440

Figure 2.

Figure 2

Overview of therapeutic modalities based on targeted degradation. (a) Targeted protein degradation approaches hijack either the ubiquitin-proteasome system or the autophagy or lysosomal pathways. RIBOTAC uses RNA-targeting small molecules and RNase L to eliminate intracellular oncogenic RNAs. Blue: ubiquitin-proteasome system; gray: autophagy pathway; violet: lysosomal pathway; pink: targeted RNA degradation. (b) Different PROTAC-based strategies are summarized. AbTac; antibody-based PROTAC; aTAG: AchillesTag; ATTEC: autophagy tethering compound; AUTAC: Autophagy Targeting Chimera; AUTOTAC: AUTOphagy TArgeting Chimera; BIAC: bispecific aptamer chimera; CLIPTAC: in-cell-click-formed proteolysis targeting chimera; CMA: chaperone-mediated autophagy; dTAG: degrader tag; GlueTac; GlueBody Chimera; G4:G-quadruplex; HyT: hydrophobic tagging; LYTAC: LYsosome TArgeting Chimera; MoDE-A; molecular degraders of extracellular proteins through the ASGPR; PROTAC: PROteolysis TArgeting Chimera; RIBOTAC: RIBOnuclease TArgeting Chimera; PHOTAC: PHOtochemically TArgeting Chimera; RNA: ribonucleic acid; SNIPER: Specific and non-genetic inhibitors of apoptosis protein (IAP)-dependent protein eraser.