The review preserves 56 imported source assertions and one official 1,066-residue product. It proposes no new GO annotation. This guide identifies the primary evidence, distinguishes repository cache availability from actual original access, and links the portable database replay.
| Source | Actual evidence used | Scope and limits |
|---|---|---|
| PMID:22664934(https://doi.org/10.3892/or.2012.1849) | Original-derived collection and mass-spectrometry Methods, plus separately recovered publisher Table II: the row identifies WDR60_HUMAN/WDR60. | The normal cache omits this target table row. Schirmer-strip collection and pooled extraction establish detection, not active secretion or an extracellular function. |
| PMID:23910462(https://doi.org/10.1016/j.ajhg.2013.06.022) | Selected original Results and Discussion: human chondrocyte ciliary-base localization and patient-fibroblast ciliation/IFT-marker abnormalities. | Residual cilia and the control-age limitation are retained; no universal initiation requirement is inferred. Some figure-caption text is absent from the normal representation. |
| PMID:25036637(https://doi.org/10.1016/j.cell.2014.05.039) | Selected full original Methods and the exact human WDR60–NUDC LUMIER record; participant ROGIDs reproduce the official sequences. | The preserved repository representation is much shorter despite its full-text flag. The fuller genuine normal retrieval was separately read. LUMIER does not prove a purified direct interface. |
| PMID:25205765(https://doi.org/10.1242/jcs.159038) | Selected full Results and Methods: human WDR34 affinity capture recovers endogenous WDR60 and light chains; endogenous WDR60 localizes around centrosomes. | NUDCD3 in this paper is not NUDC. Endogenous localization and tagged affinity capture have distinct scopes. |
| PMID:25830415(https://doi.org/10.4161/15384101.2014.985066) | Selected full Results and Methods: human endogenous WDR60/TCTEX1D2 association, cell-free translated fragment interaction and localization in cycling/ciliated cells. | Cell-free translation and coimmunoprecipitation are not a purified binary assay. Reported centrosomal, spindle-pole and cytokinetic pools are retained as contextual locations. |
| PMID:26044572(https://doi.org/10.1038/ncomms8074) | Selected full Methods and Results: human TCTEX1D2 affinity capture recovers endogenous WDR60. | A separate GFP-WDR60 transfection uses a mouse construct; a human host does not change that construct species. |
| PMID:27173435(https://doi.org/10.1038/ncomms11491) | Selected full affinity-purification Methods and exact reciprocal WDR34/WDR60 and NUDC/WDR60 records. | The study uses tagged cellular complexes. Association does not establish a physiological pathway or purified direct contact. |
| PMID:29742051(https://doi.org/10.1091/mbc.E18-03-0173) | Selected full Results/Methods and genuine supplementary construct table: human WDR60 region 473–522 binds the TCTEX1D2–DYNLT1/DYNLT3 light-chain module; target knockout/rescue changes IFT cargo distributions. | The reported velocity comparison concerns TCTEX1D2 knockout; it must not be relabeled as a WDR60 velocity measurement. Fragments and mutants are not natural isoforms. |
| PMID:30065109(https://doi.org/10.1042/BST20170568) | Selected full review sections distinguish dynein-2 assembly and ciliary cargo transport. | This is a synthesis source, not a new independent experiment. |
| PMID:30320547(https://doi.org/10.7554/eLife.39655) | Independently read full original Methods/Results: human RPE1 WDR60/WDR34 constructs, knockout, rescue and affinity capture. | The authors could not derive reliable quantitative IFT data. Anti-HA capture used DSP crosslinker. WDR60 loss permits axoneme extension with weaker complex/IFT associations; reciprocal rescue does not make the two chains interchangeable. |
| PMID:30649997(https://doi.org/10.1091/mbc.E18-10-0678) | Selected full original Results/Methods include direct human WDR60-knockout comparisons, despite the WDR34-focused title. | IFT88/IFT140 and receptor-distribution phenotypes are not a measurement of IFT velocity. |
| PMID:31451806(https://doi.org/10.1038/s41594-019-0286-y) | Independently read full original Methods/Results: recombinant human subunits expressed in insect cells, asymmetric dynein-2 architecture and structural docking to an algal IFT train. | Whole intermediate/light-chain-block deletion is not a WDR60-only deletion. Cooperative loading and tip activation are modeled; the paper does not directly measure human tip kinetics. |
| PMID:32229580(https://doi.org/10.1242/jcs.240614) | Authentic complete abstract; independent direct human subunit studies ground the positive source claims. | The cache is abstract-only. No unseen full-Methods or figure claim is made. |
| PMID:33961781(https://doi.org/10.1016/j.cell.2021.04.011) | Selected full original AP-MS Methods and literal human WDR60/DYNC2I2 records from 293T and HCT116 cells. | The preserved repository full-text representation is short; the fuller genuine normal copy was separately read. These are cellular affinity-purification associations. |
| PMID:36973253(https://doi.org/10.1038/s41467-023-37370-7) | Original nuclear Results/Methods/caption, complete original and six-supplement target-name survey, and actual Supplementary Figure 2b pixels. | The nuclear experiment resolves mouse dynein-1/dynactin reagents. The selected Y2H list also reports mouse Wdr34 (31 clones); this does not establish WDR60 nuclear localization or an exhaustive negative WDR60 screen. |
| PMID:40205054(https://doi.org/10.1038/s41586-025-08878-3) | Selected original U2OS AP-MS Methods and the original deposited NDEx network: one directed DYNC2I1-bait/DYNC2I2-prey edge. | All incident target edges are retained. Network association does not establish a purified binary interface or an isoform-discriminating interaction. |
| PMID:21530541(https://doi.org/10.1016/j.jmb.2011.04.018) | Selected full original Results and purification Methods: human full-length NUDC suppresses reporter aggregation after purification. | This independently establishes the NUDC partner class. It is not an assay of DYNC2I1 folding or chaperone activity. |
UniProt Q8WVS4 and HGNC:21862 identify DYNC2I1, formerly WDR60. The official sequence has 1,066 residues and no alternative-products block. Engineered truncations, binding fragments and disease variants are not promoted to natural isoforms.
The official PANTHER tree, alignment and PAINT IBD data reproduce the target sequence and seven literal IBD joins at PTN008562642. Its human descendant evidence includes the target itself, which is expected and not circular. The replay includes the full saved IBD file rather than a hand-written donor summary. It also preserves source-specific IntAct records from the target query, sequence checksums and the original AP-MS deposit.
The HPA target page was read at the per-location level: centrosome and primary cilium are supported, basal body approved, and cytosol uncertain. No image pixels were scored. The positive HPA cilium assertion is retained at its source scope; general centrosomal pools are not erased by more specific ciliary-base evidence. The uncertain cytosol score is not presented as an independent high-confidence soluble pool.
Six Reactome IFT events trace to Q8WVS4 residues 1–1066 in the cilium entity R-HSA-5624903 or tip entity R-HSA-5625409. The tip is core-relevant turnaround context within the main transport mechanism; these are curated model states, not new human localization or residence-time measurements. The ciliary-base and ciliary-tip closures both include cilium and do not include one another. Likewise cilium assembly and intraciliary retrograde transport are nonredundant in the saved typed closure.
InterPro IPR042505 provides the family-level electronic mapping. The current ARBA00028353 output is biologically consistent with a ciliary protein, but its current condition sets were not fully matched by the captured target cross-references; the historical execution is therefore unresolved, not falsely reconstructed. The mouse donor Q8C761 is identified independently, while direct human studies support the retained target location. The failed protein-identifier query is not treated as absence of a donor.
All existing publication-cache bytes and flags remain exact. A full_text_available: true flag does not guarantee that every table, caption or Methods section is present. In particular, the protected PMID:25036637 and PMID:33961781 representations are shorter than the separately read genuine normal copies, and the tear cache omits its identifying Table II row. These access distinctions are recorded rather than silently replacing shared files. PMID:32229580 remains abstract-only; citation correctness for its limited use is distinct from full-text availability.
The normal-fetched PMID:21530541 is the sole new publication cache proposed here. The normal-fetched metadata sources PMID:12853948, PMID:25492405 and PMID:27021811 were not used for new scientific claims and are not included in the publication payload. Existing provider output is preserved; the new provider and fallback failures are documented in the appended notes. The original notes remain an exact prefix, all 27 inherited row excerpts remain unchanged, and the four excerpts attached to the superseded cores are removed without relocation. There are no new quotations. The source-input archive contains database records, not republished paper full text.
Publisher Table II lists the WDR60_HUMAN identifier and WDR60 gene. This is the original table behind the tear-detection decision. The article's Sample retrieval, Sample processing and Data processing sections distinguish pooled Schirmer-strip extraction, mass-spectrometric identification and the separate twofold differential-abundance cutoff. The table supplies neither a target-specific peptide count nor a release mechanism. This guide remains a locator, not an independent experiment.