The source review distinguishes the biochemical action of ELANE from the identity of its substrate, experimental host and processed preparation. The normal publication caches retain their original metadata. A cache marked as containing full text does not certify that every experiment, supplement or image was inspected; conversely, selected original material was recovered for several abstract-only caches.
Each entry gives the actual access and assay boundary. The cache SHA-256 identifies the unchanged local publication file; original text copies and supplements used in the assessments are not redistributed in the database archive.
Degradation of outer membrane protein A in Escherichia coli killing by neutrophil elastase.
The authentic abstract supports E. coli OmpA cleavage and nonoxidative bacterial killing, with a separate mouse sepsis experiment. Phagosomal localization is recorded in the captured human UniProt P08246 subcellular-location annotation citing this paper, rather than stated in the inspected abstract. Operative Methods were not recovered; no exact purified preparation, imaging protocol or processed-chain sequence is authenticated.
Normal cache: PMID_10947984.md; full_text_available: false; SHA-256 7a0f1193a9f1de0f0ec67398b68086eaabb9094b7ea26f831dbe7bec1b6e82de.
Killing activity of neutrophils is mediated through activation of proteases by K+ flux.
Selected original Methods, Results and the Figure 5 caption establish human neutrophil-enzyme activity and heparin association, with separate mouse infection experiments. No figure pixels or supplement were inspected. The source supports granule protease chemistry and substrate accessibility; it does not make all infection effects an isolated human ELANE experiment.
Normal cache: PMID_11907569.md; full_text_available: false; SHA-256 4af7462d2be8596fabe13e4d73edeeeafc5693705f08c5ec592d927f92b42466.
Only the authentic abstract was recovered. UVA-associated fibroblast elastase-like activity and immunoreactivity are reported, but at least two enzymes contribute to the activity. The missing Methods prevent resolving ELANE-specific attribution; response to UV is not dismissed merely because it can involve altered enzyme production.
Normal cache: PMID_11928814.md; full_text_available: false; SHA-256 f897ba1d6bf930f9a10c8ed823d36aa7a2b216830aad00eb6d728690a2bc5763.
Selected original Methods and Results distinguish human neutrophil elastase from PR3 using synthetic serpin-derived substrates and cell-surface assays. The PAI-1 experiment here uses peptides; intact PAI-1 cleavage is attributed to an earlier paper. No figure-pixel or exact mature-enzyme sequence authentication is claimed.
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The abstract and selected original Methods/Discussion support human fibroblast CD40 cleavage and reduced CD40L-dependent IL-8/MCP-1 production, with the IL-1alpha response preserved. Complete Results and figure images were not recovered. The interaction is interpreted at substrate-engagement scope, not as purified receptor-binding affinity.
Normal cache: PMID_12223522.md; full_text_available: false; SHA-256 95c1e227e888f11f23d76fe3b7977c941d9bf5512f456d620ad56db8645ad8ab.
Recovered original Methods and Results show cleavage of recombinant human G-CSF by commercial human neutrophil elastase and reduced G-CSF-dependent proliferation. Other growth factors and proteases are explicit comparators. The authors acknowledge possible minor preparation contaminants and report a second preparation; exact enzyme termini and a binding affinity are unresolved.
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Selected original Methods and Results show human kininogen fragmentation by human neutrophil elastase using HPLC and mass spectrometry, followed by separate kallikrein assays. The prior enzyme-purification reference was not independently read for this preparation. Peptide mass assignments include ambiguities, and the findings do not establish a universal systemic anti-inflammatory effect.
Normal cache: PMID_12887060.md; full_text_available: false; SHA-256 f1a74f7c415d6132736754578f6467f21e6458816fcca69a500dc209fac7e7cf.
Selected original Methods and Results identify human neutrophil-derived elastase, recombinant human CD87 and human-cell experiments. Elastase-dependent N-terminal receptor cleavage is separated from cathepsin G-dependent C-terminal cleavage. No figure pixels, complete paper read or exact mature-enzyme termini are claimed.
Normal cache: PMID_14688365.md; full_text_available: false; SHA-256 88bc057782951b0d142594618a05e3850c5ffeb183a67353bac591cbbb700382.
The periplasmic serine protease inhibitor ecotin protects bacteria against neutrophil elastase.
Recovered original Methods and bacterial-survival Results directly test human elastase against E. coli and identify protection by ecotin. The killing preparation differs from that used for kinetic assays. This is direct antibacterial evidence; the decisive periplasmic substrate remains unresolved, and earlier OmpA work is not presented as a new experiment here.
Normal cache: PMID_14705961.md; full_text_available: false; SHA-256 6c4661630fd31bc86513d43c03d93e626f312f372226794ab8f27e39f8e342ad.
The authentic abstract reports human A549-cell IL-8 production and p38/ERK responses to human neutrophil elastase. The original body remained unavailable after bounded publisher and author-page attempts. Positive reported context is retained, without transferring Methods from the different 2006 paper PMID:16632517 or assigning kinase activity to ELANE.
Normal cache: PMID_14730209.md; full_text_available: false; SHA-256 16efc5616e94c339bc7e344fe95d8bfd35b090d7d50ef8c61de7ba9cab36bc01.
Human neutrophil-derived elastase induces airway smooth muscle cell proliferation.
The authentic abstract reports increased human airway smooth-muscle cell counts and S-phase representation after human neutrophil-derived elastase, with downstream ERK/cyclin-D1 context. The operative original was not recovered. It supports contextual proliferation, not increased cell size, an exact processed preparation or a general in vivo remodeling mechanism.
Normal cache: PMID_15010259.md; full_text_available: false; SHA-256 07f0a7cf4300919e7c948c2ce44415083672458fe6e5433fec41ce14bf417295.
Selected original mouse Methods and Results show stimulus-dependent migration and phagocytosis phenotypes. Zymosan uptake is affected in vivo, whereas in vitro zymosan uptake and in vivo E. coli uptake are not similarly reduced. No figure pixels or supplement were read. Current donor relations and the frozen human annotation relation remain separately recorded.
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The authentic abstract identifies purified human leukocyte elastase as an inhibitor of C5a-dependent chemotaxis and other neutrophil responses. Alternate-agonist controls are explicit for lysate/supernatant experiments; the purified-enzyme result is summarized as selective. Original Methods were unavailable. Acute calcium-response suppression does not resolve steady-state homeostasis, and no C5a or receptor cleavage substrate is asserted.
Normal cache: PMID_15140022.md; full_text_available: false; SHA-256 6db946b728314f30747b98956fbc07ffc6fb9ec74987c0908d38fb6e6b4e8d50.
Selected original Methods and Results separately assay human neutrophil-elastase complexes with modified alpha1-proteinase inhibitor, although the crystallographic structure contains porcine pancreatic elastase. These human experiments support the imported interaction. The porcine structure is not relabeled as human ELANE, and exact HNE processing boundaries remain unresolved.
Normal cache: PMID_16321984.md; full_text_available: false; SHA-256 eba3de423b09bb07b4319a7f4738ef249e5cb0c754b0dddd1dea9a350cc01b3f.
Selected original mouse Spi6/Elane experiments and operational cytosolic fractionation support the donor contexts. Commercial human enzyme is separately used for substrate assays and supplementation. No complete publisher PDF, figure pixels or supplement were read; distinct lysis descriptions and species/preparation limits are preserved.
Normal cache: PMID_17878334.md; full_text_available: false; SHA-256 5b0882b52cd512cd1fce137859836539dcdb1f2598b7de043354b9152c9a5eec.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
The study-linked NHLBI table identifies historical ELA2/NP_001963 with one peptide under the corresponding 2009 reference; the official P08246 record confirms that identity. Operative Methods describe pooled healthy-human urine and exosome enrichment. This supports a fraction-proteomics observation, not independently established vesicle topology, selective cargo loading or catalytic activity.
Normal cache: PMID_19056867.md; full_text_available: false; SHA-256 90ceb930bcd3ba708af5c0630dfcc028133affae4b73bd0409c758d54b43f2c4.
All operative Methods and Results in the recovered PMC article were read, with Discussion and captions but no figure pixels. Human constructs in mouse NIH 3T3 and rat RBL1 hosts are distinct from human HL-60 perturbations. The corepression and association evidence is context-specific; catalytic-dead and processing constructs are not natural splice products.
Normal cache: PMID_19506020.md; full_text_available: false; SHA-256 6c1d5ecffdc0202f90efb9c576efdcb6ad1e9cb32d50a3e5b77541597ae4e249.
Proteolysis of human thrombin generates novel host defense peptides.
Selected operative Results, Methods and captions from genuine JATS show human elastase cleavage of thrombin/prothrombin and antimicrobial activity of resulting peptides. Human neutrophil extraction and separate bacterial-protease reactions are distinguished. Mouse protection experiments apply a peptide, not ELANE. P. aeruginosa and E. coli interacting-taxon contexts remain separately preserved in the raw data.
Normal cache: PMID_20421939.md; full_text_available: true; SHA-256 5162ed2d524e6c4f5061e6c01bf9d96bead7dbf3f644b04283c13a345cbd5172.
Selected operative PMC Methods/Results and captions describe rat inflammation and BbCI treatment. The inhibitor affects elastase, cathepsin G and cathepsin L, so reduced rolling cannot be assigned uniquely to ELANE. This limits the specific transferred rolling claim without negating the observed response. No figure pixels or supplement were inspected.
Normal cache: PMID_20860667.md; full_text_available: true; SHA-256 810655f0622b93f02277bda6783dad513d10365e29e44d78f481f580fd530c69.
Neutrophil elastase and myeloperoxidase regulate the formation of neutrophil extracellular traps.
The complete scientific main text, seven main figures and six supplement pages were inspected in an independent source assessment. Human purified-enzyme histone cleavage and chromatin decondensation, human neutrophil localization and mouse knockout evidence are distinct. GW311616A also inhibits PR3, so no inhibitor-only specificity is assumed. Exact commercial enzyme sequence and termini are not reported.
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The recovered source distinguishes human neutrophil elastase cleavage of a mouse collagen-XVII fragment from separate native and disease-model contexts. The positive interaction is retained as substrate-related binding; human enzyme identity does not convert the mouse substrate or murine disease experiment into a human-human assay.
Normal cache: PMID_21979170.md; full_text_available: true; SHA-256 493b0f25e3825eb0f4289c28304403c2f09b94f7425a43f8b32901acaf5e3517.
In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.
The genuine original main article describes EPS-urine exosome-enriched preparations, but the target-specific supplemental protein/peptide table was not recovered as a valid workbook. Publisher-confirmed filenames returned error or HTML responses. The ELANE record remains unresolved without inferring absence, contamination or a false identification from the missing table.
Normal cache: PMID_23533145.md; full_text_available: true; SHA-256 f347293c23617bd56d83e1ae9bc3ad8a65e540fdbf4aff13bd0e918ec598a17e.
The authentic target workbook places ELANE/P08246 in ECM-enriched human tissue preparations with 18 distinct peptides overall. Sample-level signals are kept separate from independent-patient counts. The enrichment procedure supports contextual matrix association, not a structural scaffold function, exclusive localization or a specific active processing state.
Normal cache: PMID_25037231.md; full_text_available: true; SHA-256 7c8b582bbc01eb14e86d6099637438379bb258ca0732b645a334c456292b408c.
Operative JATS Methods, Results and Discussion were read, including captions but not figure pixels or the supplement body. Native human neutrophil observations support release of ELANE from a heterogeneous MPO-containing assembly and its cytosolic/nuclear phase. Purified actin assays and cellular kinetics are kept distinct; no invariant complex stoichiometry is inferred.
Normal cache: PMID_25066128.md; full_text_available: true; SHA-256 23f2fb835843733e1a4caea4cb7e8b20105a462b99f1d1f337873d296ebfa840.
The original supports a direct Agaphelin–human elastase interaction and inhibitory activity, while separate neutrophil and thrombosis outcomes have their own assay scope. Reported 54- and 58-residue peptide/preparation boundaries are not silently reconciled. These are experimental inhibitor constructs, not ELANE splice products.
Normal cache: PMID_25211214.md; full_text_available: true; SHA-256 90b119eeda25d29ee1b0f4cbced84fbbb9674b0aa3831a90b0582e0e5aee0c10.
Operative PMC Methods and Results explicitly identify ELANE in soluble cystic-fibrosis sputum by proteomics after removal of cells, debris and insoluble material. Separate immunofluorescence targets other proteins/glycan features, not ELANE. No supplementary target-table cells or figure pixels were independently inspected.
Normal cache: PMID_25645918.md; full_text_available: false; SHA-256 016101c5bf303d13f58f441100c5bf21b35c05f4ca76f5075befa15472466976.
Proteomic characterization of human multiple myeloma bone marrow extracellular matrix.
The authentic supplementary workbook identifies ELANE/P08246 with 16 distinct peptides overall in all 26 human marrow samples across four groups. Original and supplementary Methods establish ECM enrichment. Separate mouse histology is not treated as human ELANE evidence; the proteomic association does not establish scaffold activity or exclusive residence.
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Diverse stimuli engage different neutrophil extracellular trap pathways.
Recovered original main text, embedded supplemental captions and the author response distinguish stimulus-dependent NET formation from the measured E. coli killing assay. Candida can induce the NET response, but that does not by itself verify direct fungal killing. Source-data workbooks and figure pixels were not independently inspected, so the fungal-killing annotation remains uncertain.
Normal cache: PMID_28574339.md; full_text_available: true; SHA-256 a63097bdeed7459d389dcd61114569ffa713d5ff6fda00c07900c1eb22133940.
All five original scanned pages and Figures 1–4 were inspected in an independent source assessment. Methods specify native human purulent-sputum enzyme; the deposition source-method label is inconsistent with that account. The historical 218-residue preparation maps to current residues 30–247 with a sequence conflict, distinct from the current precursor/chain features.
Normal cache: PMID_2911584.md; full_text_available: false; SHA-256 64e0176db0ecccb27765184994c80aaa18f5da2ed69251a4e91adcfd5f0b7dad.
The operative original distinguishes human elastase processing of the SPIN inhibitor from MPO-dependent microbial killing assays. Partial inhibitor cleavage and subsequent peroxidase-related effects are not rewritten as an isolated ELANE killing assay. Human enzyme preparation and cell contexts are explicit; uninspected figure pixels or supplements are not implied.
Normal cache: PMID_29306874.md; full_text_available: true; SHA-256 80279ebb93540dc3f96307955b462f3ef0989a427d7eaba7ea1c5704ab6143d9.
Gasdermin D Exerts Anti-inflammatory Effects by Promoting Neutrophil Death.
The operative original establishes ELANE-dependent GSDMD cleavage with distinct human C268 and mouse V251 boundaries and a neutrophil death context. Direct substrate activation is retained, while the modern pyroptotic inflammatory-response term is not equated with every lytic-death endpoint or assumed ELANE-dependent IL-1beta/IL-18 production.
Normal cache: PMID_29539421.md; full_text_available: true; SHA-256 0bcf03c4ac23006fe7f8c91788bbd3ee6799dda81374aa5bbbfcd6053ce47158.
Selected operative original BioC passages include human neutrophil and recombinant human NE NET-related experiments alongside mouse knockout evidence. Species and preparation scopes remain separate. The source supports the location/formation contexts without demonstrating equivalence of all processed preparations; no additional figure-pixel or supplement reading was performed.
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Thrombus NET content is associated with clinical outcome in stroke and myocardial infarction.
An indexed copy of the published original provides human thrombus Methods, the antibody table, Results and the Figure 3C NET-localization caption. Image pixels and raw microscopy were not inspected. Elastase-positive extracellular DNA structures support location, not demonstrated catalytic activity in the specimens or a causal stroke mechanism.
Normal cache: PMID_32434865.md; full_text_available: false; SHA-256 b41353a841b69fa99918b3e47f1d3e6593387657d66c5cf3655d0118cfcb1334.
The original tests cleavage of a short synthetic SARS-CoV-2 spike activation-loop peptide. It establishes a local substrate sequence interaction and cleavage position, not direct processing of intact viral spike or a demonstrated infection phenotype. The imported interaction remains non-core with those construct limits.
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Primary structure of human neutrophil elastase.
All five original scanned pages, including sequence figures, were visually inspected. Protein sequencing concerns a historical 218-residue native preparation and glycoforms. It is not equated with the current 238-residue chain feature or represented as additional natural splice products.
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The operative original distinguishes GSDMB isoforms and protease-dependent products. ELANE cleavage/inactivation and caspase-associated products have different boundaries and consequences; the GSDMB result is not transferred to GSDMD or collapsed into a universally pro-pyroptotic ELANE function.
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Multimodal cell maps as a foundation for structural and functional genomics.
The genuine original Methods and linked AP–MS network contain an exact ELANE-bait/SERPINA1-prey edge in human U2OS cells. The tagged ORFeome assay supports a physical association or co-complex, not purified binary contact. A target insert sequence and pair-specific imaging/SEC corroboration were not independently authenticated.
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Selected original Methods, Results and captions establish human leukocyte elastase cleavage and inactivation of plasma alpha2-plasmin inhibitor and C1 inactivator. SERPINF2/P08697 is an inhibitor rather than a protease partner; the source-specific protease-binding term is therefore incorrect while its positive proteolytic evidence remains valid. No full-paper or figure-pixel claim is made.
Normal cache: PMID_6980881.md; full_text_available: false; SHA-256 930715d9a77d9626c1d9c70f8909912387c881f11943c1867cd84f60906af2b8.
The reproducible evidence archive includes the exact official responses, retrieval receipts, full saved IBD file, source contexts and offline reconstruction code. It reconstructs six PAINT joins, three current ARBA rules, seven donor queries, 51 term definitions/typed ancestry records and 21 Reactome source-row paths. Successful reconstruction verifies provenance rather than automatically deciding a biological annotation.
Gene Ontology annotation through association of InterPro records with GO terms
The captured InterPro association supports proteolysis in the target family. Official target domains and the corresponding mapping are preserved in the reproducible database archive; this is a database inference, not a new direct experiment.
Annotation inferences using phylogenetic trees
Six literal PAINT ancestral assertions lie on the human target path, with exact IBD support sets and a 267-aa MSA match. The complete saved IBD path scan contains no recorded loss. Donor and target/self evidence are valid; individual biological contexts are assessed separately from placement.
Literal UniProt subcellular-location mappings and cited experimental contexts are retained. Broad lysosomal/cytolytic labels are refined to the supported azurophil-granule compartment where appropriate, without converting all granule pools into exclusive luminal residence.
Official donor identities, complete current donor annotation queries and source-specific original evidence are preserved. Mouse NET/cytosolic contexts and rat migration/rolling contexts are not conflated; the multi-protease inhibitor leaves the specific rolling transfer uncertain.
Electronic Gene Ontology annotations created by ARBA machine learning models
Current ARBA00027399 set 18 and ARBA00090615 set 1 satisfy their captured target predicates. Current ARBA00027128 has no matching target set among 280; its historical version was not reconstructed. The extracellular location remains independently supported, so version reproducibility and biological truth are distinguished.
Combined Automated Annotation using Multiple IEA Methods
The combined electronic assertion of serine-type endopeptidase activity is consistent with the literal target family/rule records and independent human catalytic evidence. It is not treated as another primary experiment.
Degradation of the extracellular matrix
Official captured Reactome records resolve an explicit P08246 component path. The pathway R-HSA-1474228 reaches ELANE through its fibrillin-degradation event and explicit catalyst2482187, ending at P08246 entity1602474. Thus the target does some of the proteolytic work rather than merely being a matrix substrate or necessary bystander. Retain the process with the curated substrate/event-species boundaries; the pathway summary alone is not the evidence for target participation. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Elastin degradation by elastin-degrading extracellular proteinases
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-1566962 reaches P08246 through catalystActivity 2514811, physical entity 2514800 and member 1602474. This is an enzyme role, not simply presence among reaction inputs. The curated elastin model is compatible with independently established ELANE serine proteolysis; the underlying elastin paper was not independently read in this consultation. R-HSA-1566962 links its catalyst set to extracellular P08246 entity 1602474. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-1592316 follows catalyst 1602460 through protease set 1602468 to extracellular ELANE 1602474. The model separates initial proteolysis from subsequent MMP autolytic completion. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-1592398 follows catalyst 2127618 through protease set 2127623 to extracellular ELANE 1602474. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-5620971 reaches ELANE through the explicit GSDMD-cleavage catalyst in R-HSA-9710106. The owner-inspected PMID:29539421 includes direct cleavage of human GSDMD and site testing, so ELANE performs an activation step rather than merely being required for an outcome. Current GO:0070269 denotes a gasdermin-dependent inflammatory response, not every lytic death. Retain this contextual pathway assignment without claiming that the inspected study measured ELANE-dependent IL-1beta/IL-18 production, that ELANE forms the pore, or that its net inflammatory effect is universally positive. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Exocytosis of specific granule lumen proteins
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-6798749 has ELANE in the specific-granule input set and in output set 6806312 as extracellular entity 1602474. This is a transported cargo path, not evidence that ELANE catalyzes exocytosis. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. R-HSA-6798749 contains P08246 entity6800918 in specific-granule input set6799354 and an extracellular output. GO:0035580 explicitly permits elastase in this compartment, so dominant azurophilic storage is not grounds to declare this model false. The source is a curated proteomic granule assignment whose cited original was not independently read here. Retain it as an additional non-core compartment, without claiming exclusive residence or that ELANE drives exocytosis. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Exocytosis of azurophil granule lumen proteins
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-6798751 connects luminal ELANE in the input set to extracellular entity 1602474 in output set 6806184. ELANE is cargo in this event, not the exocytosis catalyst. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. R-HSA-6798751 has P08246 entity6799238 in luminal input set6798742, followed by release into the extracellular output. The literal input compartment supports a luminal pool. It does not make ELANE an exocytosis catalyst or require all stored enzyme to occupy the same intragranular microdomain. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
ELANE, CTSG or PRTN3 binds bacteria
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-6813659 includes P08246 in input set 6813639 and the output bacterial complex 6813664. This is a physical participant path; it does not independently establish a catalytic step or a new binding subtype. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-9710106 explicitly links catalyst 9710078 to cytosolic ELANE entity 9710109. Human-neutrophil fractionation independently supports a soluble cytosolic pool, and the owner-inspected PMID:29539421 reports cytosolic ELANE during aging or bacterial exposure. This is a target enzyme location, not a compartment inferred solely from its GSDMD substrate. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-9911230 places extracellular ELANE entity 1602474 in its input and ELANE-containing output complex 9911480. Association is distinguished from the separate catalytic cleavage event. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Official captured Reactome records resolve an explicit P08246 component path. R-HSA-9911236 identifies catalyst 9911491 and the ELANE-containing complex 9911480, with P08246 component 1602474. This catalyst path is distinct from the separate binding event. It supports the established enzyme activity in this curated substrate context; no new direct NOTCH2NLA experiment or autonomous signaling activity is inferred here. R-HSA-9911236 contains extracellular ELANE 1602474 within catalyst complex 9911480 and releases it as an output. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Cleavage of collagen type VIII by ELANE
Official captured Reactome records resolve an explicit P08246 component path. The exact R-NUL-2482182 model follows catalyst 2482187 to P08246 entity 1602474. The unassigned event identifier is preserved and does not erase its explicitly identified human enzyme. The source is a curated reaction model, while native-human enzyme evidence independently supports the serine endopeptidase class. R-NUL-2482182 identifies human P08246 entity 1602474 in the extracellular catalyst path. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Degradation of fibrilin-1 by Elane
Official captured Reactome records resolve an explicit P08246 component path. R-NUL-2514835 is labeled Bos taurus at the event level, but its catalyst 2482187 resolves to human P08246 entity 1602474. Preserve this substrate/event-species distinction; it is neither evidence of a wrong human gene nor proof of an intact human physiological assay. The modeled cleavage agrees with established ELANE serine endopeptidase activity. R-NUL-2514835 is a Bos taurus event with an explicitly human P08246 catalyst entity 1602474. Event species and enzyme identity must remain distinct. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
Nid1 degradation by MMP1, 9, 12, ELANE
Official captured Reactome records resolve an explicit P08246 component path. R-NUL-2533972 follows catalyst 2533962 through physical entity 2533968 to human ELANE member 1602474. The target is therefore represented as a catalyst, not merely a cleaved substrate. This curated substrate context is compatible with established enzyme activity; the cited nidogen originals were not independently examined here. R-NUL-2533972 reaches extracellular P08246 entity 1602474 through catalyst 2533962 and protease set 2533968. The modeled compartment agrees with independent human ELANE release evidence; this review does not relabel the model as a newly inspected primary assay or require exclusive extracellular residence. This assessment verifies the database representation; underlying primary papers are not claimed read unless separately assessed.
The 102 normal source objects and all 104 raw QuickGO contexts are retained. Two pairs differ in interacting taxon even though that field is deduplicated by the normal TSV projection; those raw biological contexts remain visible in the archive. There are no newly proposed annotation rows or publication quotations.
The official P08246 product is a 267-aa precursor without an alternative-products block. Signal, propeptide and chain features describe processing, not natural splice products. Historical 218-aa enzyme preparations, glycoforms and engineered constructs are documented at their own boundaries; equivalence to every current processing state is not assumed.
The three added core location identifiers are current cellular components in the saved official QuickGO records: azurophil granule, phagocytic vesicle and neutrophil extracellular trap. Their is_a closures reach cellular anatomical entity and do not classify them as protein-containing complexes.
The generic process proteolysis covers peptide-bond cleavage. Its four ACCEPT decisions are preserved; the compact core already states the enzyme chemistry through GO:0004252 and lists selected biological contexts. This is a choice of summary granularity, not a claim that a molecular-function term is a biological-process ancestor or that all accepted processes must be duplicated in the core.