The review separates the catalytic function from interaction, clock and EV claims. The source guide explains access limits; source evidence pins current excerpts and the archive.
PMID:32019926(https://doi.org/10.1038/s41467-020-14524-5), selected original Methods/Results: human isoform 2 has an internal His6 insertion between Gly299/Asp300 and Sf21 expression. Glutamate and glucosamine-6-phosphate have separate coupled readouts; UDP-GlcNAc interference restricts inhibition measurement to the former. The inspected phosphosugar identity is ambiguous; substrate kinetics and separately curated features support specificity. The reported human structure forms an asymmetric homodimer.
PMID:35229715(https://doi.org/10.7554/eLife.69223), selected original Methods/Results: recombinant human GFPT1 is an assayed comparator despite the title. Human GFPT2 activity independently establishes the partner class considered during interaction review. Mouse embryonic-stem-cell findings are separate from human GFPT1 physiology.
PMID:11679416(https://pubmed.ncbi.nlm.nih.gov/11679416/) reports a muscle-enriched splice insertion and a recombinant kinetic comparison; the complete reagent crosswalk is unresolved. The official 699/681-residue sequences are distinct from engineered tagged reagents. PMID:1460020(https://pubmed.ncbi.nlm.nih.gov/1460020/), original main text inspected through an indexed author-paper mirror, establishes recombinant human chemistry. OCR and uninspected figure pixels limit fine numeric claims.
The official Q06210 record lists F6P BINDING features at 394/395/439–441/444 with ECO:0000305/PMID:19059404 and ECO:0007744/PDB:2ZJ3. These are curated inference/structure annotations, not a newly inspected F6P-binding experiment. UDP-GlcNAc is a separate directly supported feedback ligand. No specific UDP-GlcNAc-binding GO descendant was established in the bounded term search. Engineered tags and mutants remain assay reagents, not additional natural products.
| Study | Literal target evidence | Scope |
|---|---|---|
| BioPlex, PMID:33961781 | Official BioPlex3 row 74587: GFPT2 bait / Q06210-2 GFPT1 prey | HEK293T AP-MS; GeneID parsimony prevents isoform-specific inference |
| MuSIC2, PMID:40205054 | Original edge 606018: GFPT2 bait / GFPT1 prey, exact Ensembl-node joins | Tagged U2OS AP-MS; no independent binary or physiological heteromer claim |
The positive association and the partner's catalytic class are different evidence claims. No GFPT2-specific role is transferred to GFPT1.
PMID:23395176(https://doi.org/10.1016/j.cmet.2012.12.015), selected original main text: human U2OS-B6 GFAT1 knockdown reduces Bmal1/Cry1 expression. GFPT1 supplies hexosamine intermediates; OGT performs clock-protein modification. The rhythmic reporter targets OGT, while mouse Gfat1 itself varies at approximately 12 hours. This supports contextual regulation without establishing GFPT1-specific period/phase effects. Supplementary assays and figure pixels were not inspected.
PMID:20458337(https://www.researchgate.net/publication/44588150_MHC_class_II-associated_proteins_in_B-cell_exosomes_and_potential_functional_implications_for_exosome_biogenesis), original Methods/Results: human RN B-cell EV preparation; ExoCarta experiments 79/80 separately identify GFPT1/Q06210 by MS. Original peptide tables remain inaccessible. CL:0000639 is a pituitary basophil. Preserve this conflicting literal extension; no presumed B-cell replacement is made.
Actual PTHR10937 tree/alignment replay places human AN67/PTN002475099 below the catalytic and UDP-biosynthesis AN6/PTN000101302 assertion, and below F6P-metabolism AN14/PTN000859281. Literal experimental donors, including human self evidence, are retained; the two IKR records are off-target.
The actual expression, mutant and normal reaction paths reach human Q06210 residues 2–699 in cytosol. The normal catalyst is an alternative set containing GFPT1 and GFPT2, not proof of a heteromer. Disease-event titles do not negate wild-type chemistry. These are curated model assertions, not fresh localization experiments.