Protein degradation spans the ubiquitin–proteasome system (UPS) and autophagy–lysosome routes—central hubs for proteostasis and signal resetting. We provide tools for ubiquitin/ligases, p97/VCP, autophagy markers, and PROTAC-oriented readouts from basic regulation to targeted protein degradation (TPD).
Focus areas: E3 substrate recognition & CRL dynamics, ERAD–p97 axis, selective autophagy receptors, rational PROTAC/molecular-glue design
Commonly used for mechanistic studies; follow your lab SOP, compound datasheets, and ethics approvals.
| Compound | Targets / pathways | Experimental notes |
|---|---|---|
| MG132 | Proteasome (reversible tool) | Common UPS-dependency probe; cytotoxic—tightly window dose and time. |
| Lactacystin | Proteasome (irreversible; β-subunit–related) | Relatively clean proteasome tool; still cytotoxic—pair controls. |
| MLN4924 (Pevonedistat) | NEDDylation / NAE1 | CRL-axis intervention; mind cell-cycle context and substrate differences. |
| Chloroquine | Lysosomal acidification (autophagic flux block) | Often paired with BafA1 to stage flux; mind cardiotoxicity literature. |
| Bafilomycin A1 | V-ATPase / lysosomal acidification | Blocks downstream fusion/degradation steps; potent—mind vehicle and nM doses. |
| 3-Methyladenine | PI3K class III (autophagy initiation–related) | Classic but promiscuous—better for coarse modulation than single-mechanism claims. |
| CB-5083 | p97 / VCP ATPase | ERAD/stress-granule contexts; watch mitochondrial/cell-death phenotypes. |