COG7 supplies a COG5-contacting structural interface in lobe B of the COG complex. Original reconstruction uses human cDNAs in rabbit reticulocyte lysate: COG5 and COG7 together promote COG6 incorporation, with the lobe-B subunits supporting optimal COG8 incorporation. Possible endogenous factors limit claims of purified binary directness. The original COG5-pair assertion is refined to GO:0140378 protein complex scaffold activity; other COG associations remain separately represented. There is one integrated core and no NEW annotation. PMID:15047703
The later structure uses K. lactis fragments. Separate human COG7 interface tests show impaired COG5 association for N-terminal deletions and the I17/F21/V41-to-Asp mutant. That mutant reduces recovered lobe-B assembly about twofold; it does not cause a claimed complete collapse. Glycosylation-rescue experiments test COG5 mutants, not a COG7 rescue construct. These distinctions support a COG7-specific assembly interpretation without importing COG4's independently demonstrated bridging mechanism. The official scaffold definition and its three specialized descendants were read; ubiquitin-ligase, MAPK and centriole scaffold terms do not fit this activity. PMID:25331899
COG7–Sly1 association in the original source is positive but weak. The Methods identify recombinant rat Sly1, matching the Q62991 source partner. Human-host identity does not convert that construct into human SCFD1. COG4-specific purified binding and syntaxin coordination are not assigned to COG7. The missing exact pair in the queried interaction export is not negative evidence against the original experiment. PMID:19536132
Original human COG7 localization uses a 770-residue tagged construct in HeLa cells; the separately purified bovine COG complex is a different experimental scope. The current P83436 sequence is 770 residues and no alternative products are seeded. Length agreement alone does not authenticate the historical clone sequence. The exact protected normal abstract stays unchanged; a genuine fuller normal variant remains separately archived and was assessed within the core consultation. PMID:11980916
The original COG7 patient study was recovered from its publisher as full HTML. Two affected infants and their fibroblasts exhibit altered trafficking and glycosylation, with wild-type human COG7 complementation. Residual COG7 and differences between the patients' individual sugar-transport and transferase assays are retained. Cathepsin-D transport was not uniformly defective. COG7 contributes the structure and organization of trafficking machinery; no intrinsic glycosyltransferase or sugar-transport activity is assigned. The two glycoprotein-biosynthesis assertions remain contextual non-core participation through Golgi enzyme positioning. PMID:15107842
The 2006 recycling paper is COG3-centered, but its actual COG7-depletion section was recovered through an indexed original Wiley response. Human COG7 knockdown changes GlcNAcT1/GS15 distribution, Lamp2 glycosylation and selected protein abundance. Much of the time course and the isolated-vesicle experiment concern COG3 and are not transferred to COG7. The downloaded normal cache remains abstract-only; the selected original Results, Figure 5 legend, Discussion and RNAi/cell-culture Methods are accessible separately. No Figure 5 pixel inspection or complete downloaded article is claimed. PMID:16420527
In COG7-deficient patient fibroblasts, BFA-induced redistribution of Golgi proteins toward the ER is delayed and corrected by COG7. Coat release is not detectably impaired and anterograde redistribution is less affected. ERGIC-53 and selected SNAREs are mislocalized. GS15 abundance is reduced and restored after complementation. Tested proteasomal/lysosomal inhibitors do not restore GS15, and the authors leave the depletion mechanism unresolved. The two source-specific stabilization assertions are retained as qualified ACCEPT: the broad definition permits complex-mediated maintenance, supported by selective abundance/localization changes and COG7 correction. The molecular protective step and turnover pathway remain unresolved. No intrinsic chaperone chemistry is required, and inhibitor failure does not refute a trafficking-mediated maintenance role. The original COG3/COG7 double-knockdown result is kept distinct from COG7-only perturbation. PMID:16510524
The complete human knockout study independently establishes COG7-dependent partner abundance and EM abnormalities. Light-microscopy markers can remain perinuclear despite abnormal dilated cisternae. Toxin assays use representative knockout subsets, so general results are not presented as verified COG7 measurements in every panel. COG7-specific assembly, clinical and depletion evidence supports retained transport and Golgi organization. PMID:27066481
All 14 original binding assertions remain represented. The two full exports contain 113 complete 42-field records, with 31 exact target–paper–partner occurrences. One rat-Sly1 assertion lacks an exact export record but has actual original-paper support. Records preserve species, host, experimental roles, feature strings, sequence checksums and negative flags. A repeated interaction accession is not alone a deduplication key across partners.
The campaign policy in projects/CLINGEN_MENDELIAN.md retains experimentally supported generic binding as non-core when no informative exact class is established. This overrides the generic skill's default removal of uninformative binding. Class refinements describe the bound product and do not transfer its biological role to COG7. There is no inference that every Y2H pair occurs natively in a Golgi complex.
The MEOX2 source Q6FHY5 is a 303-residue product, differing from canonical P50222 by one glutamine in a poly-Q segment while retaining the homeobox. It is not silently replaced by the canonical identifier or confused with separately annotated histidine-deletion variants. Its DNA-binding transcription-factor class is a qualified inference from the reviewed reference product and exact sequence relationship; the screen does not measure that variant's transcriptional activity. PMID:26871637
KIFC3/Q9BVG8-5 is named isoform 4 in the official record, illustrating why the accession is used for exact scope. Its 687-residue reconstruction and six record checksums match, and the entire motor domain is retained. Kinesin binding refines the two positive assertions without assigning ATP hydrolysis or movement to COG7. TAX1BP1 pairs remain positive non-core. The variant-interaction record contains a COG7 residue-749 feature marked as having no effect; it is not described as a featureless wild-type assay. [PMID:26871637; PMID:32296183; PMID:31515488]
The innate-immune source maps human COG7 to mouse TRAF5 in a human host. BioPlex supplies four target-paper records across COG4 and COG5, two per partner in HEK293T/HCT116 contexts. Those are co-complex measurements rather than purified affinity. The selected 21903422, 25416956 and 33961781 bodies have Introduction/Discussion context; target provenance is supplied by exact complete interaction records, without a false claim to read absent Methods. HuRI-wide orthogonal validation is not assigned to each target pair. [PMID:21903422; PMID:25416956; PMID:33961781; PMID:32296183]
Six exact current donor/target joins contain 17 same-term records. Fly Cog7 experiments demonstrate rescue, altered COG5 stability and Golgi morphology; plant EYE experiments provide their own localization/Golgi premise. Their developmental contexts are not manufactured as human functions. The fly Rab-proteomics paper was read for actual assay context, but its specific Cog7 supplementary target row remains uninspected; that link is UNVERIFIED rather than falsely claimed as independently authenticated. [PMID:22946051; PMID:18422605; PMID:25453831]
PTN000484904 remains UNRESOLVED at the historical source-entity level because the tree/alignment/IBD placement was not inspected. Current positive extant records and human structural evidence support the target judgments independently. Donor count is not a confidence proxy; the target's own experimental descendant evidence is legitimate, not circular. Current plant qualifiers and all original source fields are preserved exactly.
The nine current Reactome events resolve through compartment-specific COG complexes to COG7 reference entity 52524/P83436. Golgi and TGN locations remain source-specific; event membership does not assign Rab activity, coat removal or autonomous SNARE fusion to COG7. The RAB6 event explicitly allows distinct GARP and COG populations. The current HPA XML supports Golgi localization without adding incidental locations as new assertions. No target GO-CAM entry was found in the protected index; this absence is not treated as a missing-function claim.
Genuine isolated fetch produced 46 source assertions from 47 raw GOA occurrences, with one duplicated semantic assertion; all remain covered. No products are seeded, and all 26 original reference ID/title pairs are preserved. Four genuine supplemental references are added. Exact current-main publication, Reactome and GO-CAM sources remain protected; genuine normal alternatives are separately archived. Shared absent-main sources will be compared against actual published heads at the finite application guard.
The real Falcon request timed out and the configured perplexity-lite fallback returned an insufficient-quota error. No provider report was fabricated. Manual primary readings and three bounded independent consultations supply the assessment. The owner ledger records actual complete selected paragraphs and indexed windows; the consultations retain their separate additional reading scope. Two short genuine primary anchors occur once in YAML and are not repeated here or in the provenance index.
The source index records provenance and assay limits; it is not primary scientific evidence. No canonical file, Git state, existing history or remote was edited by this owner. A separate immutable first-draft snapshot retains the initial accession-number wording; subsequent narrow changes are recorded explicitly.
Genuine isolated normal2 validation, status checking and rendering all passed. The calculated status remains DRAFT with 11 advisories: ten supported generic-binding retentions follow the explicit campaign policy, and the current official GO:0017119 label is COG complex while the validator uses the older Golgi transport complex label. No machine-sourced ID/label was rewritten to silence that ontology-version warning. The current official core label is retained.
The first draft and its next accession-precision snapshot remain archived. Final scientific changes comprise two KIFC3 summary clarifications using Q9BVG8-5 and two stabilization decisions changed from provisional UNDECIDED to qualified ACCEPT after independent reading of the actual definition and source passages. All original assertion objects, reference identities, product absence and the single scaffold core remain unchanged. The final source guard covers 14 additions and 23 protected paths at main 982283782408ae93275a20473e4560c61223ab56. Four shared-source occurrences match exact published COG4, COG5 and COG6 blobs. The complete 379-PR inventory is clear for COG7 and its ORF/secondary aliases; live publisher application remains ROOT-only.
The closing check detected an unrelated main advance and retained the stopped receipt. Incremental requalification at 24547fdaadbba48b20d24a122e8d67341f44ae22 covers 376 complete open PR inventories, with all 14 additions/23 protected sources and the four shared blobs unchanged. The only tooling-tree change is one added fungal GO:0070879 cache row; authenticated old/new blob comparison proves every previous byte-line unchanged, no COG7 term overlap and no validator-code change. This final applicability record supersedes the earlier snapshot for source application; the normal2 scientific checks remain valid with their original tooling provenance.
The COG7-specific Results and Figure 5 legend in the 2006 recycling paper were reread. GM130 and syntaxin-5 loss is explicitly reported for COG7 knockdown versus mock or COG3 knockdown, with the short Golgi form more affected. The source index now provides a short literal excerpt, DOI, public original URL and exact saved-text locator. This separate external text does not change the abstract-only repository cache or imply figure-pixel inspection. The combined COG3/COG7 GlcNAcT1 result remains a double perturbation. PMID:16420527
The human COG7 interface is “essential for the assembly and/or stability of COG5–COG7 complexes”. The interface experiments measure association and recovered assembly; they do not measure total COG8 abundance. Independent COG7 knockout immunoblots show lobe-B partner loss, and patient-cell COG7 correction restores GS15. Protein stabilization is therefore now explicit within the existing scaffold core, at complex-mediated maintenance scope. Neither a direct protective contact with every resident nor an identified degradation pathway is asserted. Glycoprotein biosynthesis remains contextual non-core participation because its named chemistry is glycan formation by other machinery. [PMID:25331899; PMID:27066481; PMID:16510524]
The MEOX2 and KIFC3 binding refinements depend on the identity and class of the exact positive partner, not the number of papers or a presumption of native colocalization. Array, pooling and validated-two-hybrid records are stages of the same screening approach, not independent biological replications. The Q6FHY5 MEOX2 product retains the reviewed reference homeobox with one poly-Q deletion; the reference's experimental RNA polymerase II-specific transcription-factor class supports GO:0061629. This is a stated product inference, not an activity assay of Q6FHY5. All six KIFC3 records map the same reconstructed Q9BVG8-5 with an intact motor domain; their natural-isoform confirmation caveat remains. TAX1BP1 retains positive non-core binding: its established adaptor/receptor functions do not themselves supply an applicable more-specific binding class. A mapped contact domain is not required for partner-class refinement. [PMID:26871637; PMID:32296183; PMID:25416956; PMID:31515488]
This appendix supersedes the earlier broad MEOX2 replacement and makes the previously accepted stabilization scope explicit. All original sources, actions, product absence and historical reference identities remain unchanged. There is still one scaffold core and no NEW annotation. Earlier access and validation sections above remain dated provenance; the present source index separates the finite correction from those historical records.
Ordinary follow-up validation, dry-run status and rendering passed with the same 11 advisories: ten supported generic-binding retentions under the campaign policy and the validator's older label for the COG complex. The current official label is retained. The external PMID16420527 excerpt was checked separately against the original returned text; the normal publication-cache validator is not presented as validating that separate source.