The core is lysosomal glucosylceramide hydrolysis (GO:0004348), directly contributing to glucosylceramide catabolism (GO:0006680) and ceramide formation (GO:0046513). Saposin-assisted access to membrane lipid and the lumenal catalytic setting are compatible; membrane association does not make GBA1 a transmembrane transporter. Natural-substrate liposome work and cellular salvage experiments independently ground the core. The latter separates GBA1 cleavage from subsequent acid-ceramidase and ceramide-synthase steps. PMID:9201993(https://pubmed.ncbi.nlm.nih.gov/9201993/); PMID:19279011(https://pubmed.ncbi.nlm.nih.gov/19279011/).
Secondary glucosyl transfer and steryl-glucoside hydrolysis are retained without assuming a fixed net direction in every cell. Original PMID:26724485 Discussion supports baseline degradation and cholesterol-loading-dependent formation, but leaves the causal consequences of altered glucosylcholesterol in Gaucher disease unresolved; the structured biology gap is limited to that question. The accessible PMID:24211208 abstract concerns GlcCer-dependent synthesis, whereas selected original PMID:26724485 Methods/Results distinguish hydrolysis and transfer and distinguish GBA1 from the mouse GBA2 comparator. The former's uninspected Methods are not reconstructed from its abstract. PMID:24211208(https://pubmed.ncbi.nlm.nih.gov/24211208/); PMID:26724485(https://pubmed.ncbi.nlm.nih.gov/26724485/).
Three additional sources qualify substrate breadth. The external original PMID:32144204 Results accompanying Fig. 9E state: “GalCer hydrolysis occurred in the presence of rGBA1”. Its C6-NBD-GalCer assay gives approximately 200-fold lower activity than the GlcCer analog. This is not a comparison with GALC. The official human GALC record establishes a lysosomal GalCer hydrolase associated with Krabbe disease. The positive GBA1 assay remains valid, while physiological GalCer clearance by GBA1 is unestablished and the annotation is marked over-annotated. PMID:33361282 supports xylose-containing lipid chemistry. PMID:39395789 main-text paragraph27 distinguishes sterol substrates from fluorogenic probes and explicitly allows poor solubility to limit 6-O-palmitoylated substrate degradation. No medaka result is attributed to the last paper. PMID:32144204(https://pubmed.ncbi.nlm.nih.gov/32144204/); PMID:33361282(https://pubmed.ncbi.nlm.nih.gov/33361282/); PMID:39395789(https://pubmed.ncbi.nlm.nih.gov/39395789/).
The GO:0009247 definition describes diacylglycerol glycolipids, yet actual typed children include glycosphingolipid, dolichol-linked and galactolipid biosynthesis. The three non-core sterol-glycoside synthesis contexts retain this ontology-scope question explicitly. GO:0046527 does not require UDP-glucose; no unverified specific child or new physiological pathway is invented. Current definitions and typed-child evidence are preserved in the source archive.
LIMP-2/SCARB2 and chaperone partners support informative partner-specific binding refinements. The original PGRN interaction remains positive, while its generic protein-binding row is removed for informativeness. PGRN recruitment of HSP70 does not independently establish that PGRN itself meets the folding-chaperone class required by GO:0051087. PMID:18022370(https://pubmed.ncbi.nlm.nih.gov/18022370/); PMID:25202012(https://pubmed.ncbi.nlm.nih.gov/25202012/); PMID:27789271(https://pubmed.ncbi.nlm.nih.gov/27789271/).
PMID:40159502 selected structure/Methods use soluble LIMP-2 residues 36–431, not the native bilayer-spanning receptor. The interface supports binding; native topology, low-pH release and a simultaneous saposin complex require distinct evidence. ER/Golgi/TGN localization can accompany delivery without becoming GBA1's principal catalytic compartment. PMID:40159502(https://pubmed.ncbi.nlm.nih.gov/40159502/).
The actual official Reactome participant chain is reaction 1605591 → GBA1:SAPC catalyst 1605675 → human GBA1 entity 1605775, linked to P04062 chain 40–536 at the lysosomal membrane. These are inspected official HTML participant links, not an inferred membership from a reaction title or successful ContentService JSON. Imported GO columns on the entity are not additional experiments.
The protein-clearance, autophagy and lysosome-organization annotations retain positive effects while separating endpoints from executed chemistry. PMID:26392287 uses human GBA1 in rodents; that host does not make the construct wrong-target. Static LC3/p62 cannot resolve induction versus blocked clearance. PMID:27378698 reports cell-type-dependent flux and lysosome-reformation endpoints, leaving parts of the lipid/signaling mechanism unresolved. Lack of a protease activity alone is not the reason for the two direct protein-catabolism over-annotation decisions. PMID:26392287(https://pubmed.ncbi.nlm.nih.gov/26392287/); PMID:27378698(https://pubmed.ncbi.nlm.nih.gov/27378698/).
PMID:23707074 Results (Fig.3) and live-cell Methods measure mitochondrial potential with TMRM in mouse neurons and astrocytes, including oligomycin responses. This supports the specific GO:0051881 replacement for the broader potential term, without a direct membrane-pump assignment. PMID:23707074(https://pubmed.ncbi.nlm.nih.gov/23707074/).
PMID:25456120 includes wild-type biochemical controls but twin-only MEA comparisons. Protein/dopamine rescue is not firing rescue. Its full main text is accessible. The two NOT contexts remain bounded culture observations; the firing annotation remains UNDECIDED because the inspected comparison does not isolate GBA1-dependent firing relative to wild type, not because the main paper is inaccessible. The protein-abundance result supports regulation without directly measuring degradation rate. Main figure pixels and full supplementary methods were not inspected. PMID:25456120(https://pubmed.ncbi.nlm.nih.gov/25456120/).
PMID:9101438 selected original Methods/Results/Discussion concern rat epidermal enzyme responses and lipid-barrier maturation. The Results on p. 580 state that “activity was unaffected by 1 d of DHT treatment”; after two days, GCase activity was “75% of control”. These DHT-specific findings differ from the abstract’s summary of accelerating hormones. CBE impairs extracellular lipid maturation despite substantially preserved lamellar bodies and secretion, supporting direct catalysis in barrier establishment. Human rows remain donor transfers, not human hormone assays. External original article.
PMID:23580063 now has genuine full text. Selected Methods/Results distinguish strong enzyme inhibition from bounded alpha-synuclein and proteolysis results; rat neuronal proteolysis was not measured. A 2021 correction addresses Fig.6A beta-actin band removal and supplies a corrected panel. It announces no revised enzyme assay. Figure pixels/raw blots were not reanalyzed. PMID:23580063(https://pubmed.ncbi.nlm.nih.gov/23580063/).
Authentic PMID:23533145 Supplementary Table 2, sheet SI Table 2, header row 6 and data row 626 identifies P04062 / Glucosylceramidase / GBA. The literal unique-peptide counts for EPS Exo PCa1, PCa2, NC1 and NC2 are 1,0,5,5; corresponding LFQ intensities are 0,0,25059000,38052000. The two measurements are analyses of pooled clinical samples, not independent donor replicates. The main Methods describe pooled EPS-urine fractionation and mass spectrometry; the Discussion acknowledges co-isolation and soluble contaminants. This establishes fraction detection, not vesicle topology, a biogenesis role or product-exclusive localization. PMID:23533145(https://pubmed.ncbi.nlm.nih.gov/23533145/).
The workbook identity is NIHMS502285-supplement-Supplemental_Table_2.xlsx, SHA256 6c76b1cd34e709839d8353a5c1584118f0a0c99d8edbfaf361bd1f275f896a70. Literal header/value extraction is retained with the source evidence. No figure-image or donor-level peptide inference is made.
Official P04062 version 277 declares five sequences of 536/516/263/449/487 residues, each independently matched to direct FASTA and coordinate reconstruction. The first two arise from alternative initiation, not an invented splice mechanism. PMID:3687939 supports active lysosomal products under its tested conditions. The PMID:8294033/ENA D13287 pseudogene provenance raises a specific uncertainty for product 3: BAA02546.1 is also 263 residues but differs at nine positions. This is neither an established identity nor grounds for deleting an official product. Functions of products 4/5 remain unverified in the selected evidence; this access boundary is not promoted to a field-wide claim that nobody knows. A SUSPECTED/CHECK source-record concern makes product 3 provenance queryable without a deletion or replacement claim. PMID:3687939(https://pubmed.ncbi.nlm.nih.gov/3687939/); PMID:8294033(https://pubmed.ncbi.nlm.nih.gov/8294033/).
Actual PTHR11069 tree/MSA data place the sequence-identical human AN30/PTN002476139 below AN7/PTN001667738 for both incoming IBA assertions. The two IBD donor sets match the raw records, including legitimate target self-evidence. No NOT/IRD/IKR exception was found. The literal ancestral metadata Eubacteria/taxon 2 is retained as family-record provenance, not assigned to human or interpreted as an independently dated evolutionary event. These two specific assertions do not establish every secondary substrate or truncated-product activity.
The cache flag describes the repository copy. The review field full_text_unavailable describes actual access, so it is not set merely because a cache contains an abstract when selected original text was read elsewhere. PMID:18022370 already has that flag and remains abstract-only. External readings below cover the named sections, not every figure image or supplement.
| PMID | Repository copy | External original and inspected locator |
|---|---|---|
| 32144204 | Abstract only | Results accompanying Fig. 9E; substrate Methods; Rendered lines 309–311 and 454–457. |
| 9101438 | Abstract only | Results, article p. 580; selected Methods and Discussion; Rendered lines 1900–1932; original Results and Fig. 5 discussion. |
| 21098288 | Abstract only | Selected Results and Fig. 4 caption; Rendered lines 203–223. |
| 19710420 | Abstract only | Selected Methods and Results, Table 1; Rendered lines 190–213; beta-glucocerebrosidase row 213. |
| 18022370 | Abstract only | No full original inspected; full_text_unavailable: true remains. |
| 19279008 | Abstract only | Selected Methods, Results and Discussion; Methods 119–167; Results 184–195 and 242; Discussion 260–266. |
| 19279011 | Abstract only | Selected Methods, Results and Discussion; Methods 148; Results/Discussion 157–203. |
| 25202012 | Abstract only | Selected Methods and Results; Methods 118; Results 164–166. |
| 26392287 | Abstract only | Selected Methods 2.2/2.3/2.5, Results 3.1–3.3 and Discussion; Publisher-layout article text and figure captions; no figure-pixel reanalysis. |
The primary target is GBA1. The older GBA namespace and all eight pre-existing history objects remain unchanged. All 190 historical annotation occurrences, 97 historical context keys and 366 old quotation associations retain original blob/hash/pointer identities. Current 96 decisions are separately authored; the GBA-only historical row is not added as NEW. The two old NTRs are retired explicitly: compartment can accompany existing GlcCer catabolism, and GBA1's lysosome-reformation mechanism remains a question rather than a dedicated new process claim.
Three single-group extension atoms are restored in the native review, using BFO:0000066 (occurs in). Raw 76's two alternative groups each pair has_input UniProtKB:P37840 with a different occurs_in UBERON value. The common has_input P37840 atom is entailed by both alternatives and is now projected once as RO:0002233. This is a partial consequence, not an equivalent encoding: the flat schema cannot express the alternative locations. Both literal groups remain in the archive; the locations are not flattened into a conjunction and no additional original is manufactured.
The 44 reference assessments distinguish cached abstracts from separately inspected original text. Seven review quotations retain exact normal-cache byte offsets. Three short guide excerpts from external originals have separate source URLs and normalized-text offsets; they are not attributed to abstract-only caches. Aggregate quotation budgets remain at most 25 words per source. The evidence archive preserves the 96 current original contexts, historical identities and source-access records, including the full alternative extension groups. Baseline acquisition and validation provenance remains explicitly scoped to the published parent; current session outcomes belong in history.
The specific skin-barrier relationship is GO:0061436 is_a GO:0098773. Both the retained initial official response and the follow-up response verify this edge. The broader development row remains TOO_GENERAL.