| Year | Study (first author) | Publication type | What’s new (1–2 sentences) | Relevance to CAND2 (direct/indirect) | Key data/metrics | URL/DOI |
|---|---|---|---|---|---|---|
| 2024 | Zhang | Review | Synthesizes the current neddylation field and reiterates the core regulatory logic that CAND proteins bind unneddylated cullins, while CSN-mediated deneddylation restores a CAND-accessible state. This is useful pathway context for interpreting how human CAND2 should function within CRL cycling, even though the review focuses mainly on CAND1. (pqac-00000013) | Indirect | Describes structural precedents for CAND1-cullin complexes and the CAND/CSN/NEDD8 cycle; no CAND2-specific quantitative dataset reported in the extracted context. (pqac-00000013) | https://doi.org/10.1038/s41392-024-01800-9 |
| 2024 | Wang | Primary research (Nature Structural & Molecular Biology) | Shows that CAND1 can inhibit CRL2 assembly/activity rather than simply acting as a universal exchange activator, refining the broader CRL regulatory model. This is important for CAND2 annotation because it argues that CAND-family effects are cullin-context dependent, not uniformly activating or inhibitory. (pqac-00000015, pqac-00000016, pqac-00000017) | Indirect | For CUL2·CAND1, neddylation increased dissociation ~5-fold, shortening t1/2 from ~20 min to ~4 min; MLN4924 stabilized a CRL2 substrate, and CSN inhibition mildly enhanced degradation in the reported system. (pqac-00000015, pqac-00000017) | https://doi.org/10.1038/s41594-023-01167-5 |
| 2023 | Xie | Commentary/News & Views-style article | Highlights 2023 advances establishing CAND1 as a dynamic CRL assembly/disassembly factor and explicitly notes that CAND1 and its homolog CAND2 can be viewed as exchange-factor-like regulators. It does not add new CAND2 experiments, but it frames how the field interprets CAND-family function. (pqac-00000000) | Indirect | No new primary CAND2 metrics in the extracted context; conceptual emphasis on exchange-factor behavior of CAND-family proteins. (pqac-00000000) | https://doi.org/10.1016/j.cell.2023.04.001 |
| 2023–2024 | No direct human CAND2 primary study identified in the provided 2023–2024 context IDs | Evidence gap statement | Within the provided 2023–2024 context, no direct primary study on human CAND2 itself was captured; most recent evidence is pathway-level or CAND1-centered and therefore must be used cautiously for inference. The strongest direct mechanistic human CAND2 study in the available context is from 2025, outside the user-prioritized 2023–2024 window. (pqac-00000000, pqac-00000013, pqac-00000015, pqac-00000016, pqac-00000017) | Direct evidence lacking in 2023–2024; indirect inference only | Key implication: current 2023–2024 annotation of human CAND2 relies mainly on CAND-family/CRL-cycle context rather than new CAND2-specific experiments in the provided evidence base. (pqac-00000000, pqac-00000013, pqac-00000015, pqac-00000016, pqac-00000017) | n/a |


*Table: This table summarizes the most relevant 2023–2024 studies in the provided evidence base for interpreting human CAND2 function and pathway context. It also makes explicit that direct human CAND2 primary evidence was not captured in the provided 2023–2024 contexts, so recent annotation depends largely on indirect CAND-family and CRL-cycle studies.*