2026-09-29. Manual source notes for the prospective review of all 127 imported source assertions. Row numbers below are one-based. These notes are not a provider-generated report or a normal publication cache. No canonical review was edited.
The deterministic primary import contains 127 distinct projected source tuples and null products. The raw API count was 128; the absent original API response prevents a claim about the reason for that earlier collapse. The YAML, GOA and UniProt preimages are preserved in the research baseline. The sole normal research command failed after 4.95 seconds and generated no report. Its structured receipt preserves the actual child exit code; keyword signals in the discarded diagnostic do not establish a more precise failure cause.
All 15 staged publication abstracts and the two staged Reactome summaries were read. Seven absent publications were independently identity-checked and subsequently imported exclusively under the separate Seed29 source procedure. Ten existing canonical records remain unchanged, including the eight shared records previously imported by Seed28. The differing staged versions of PMID24769233 and PMID30280653 remain quarantined. The latter was read as a separately identified source version, not silently substituted for the shorter canonical cache. All primary figure-pixel and supplement inspections remain unclaimed.
PMID18728015, original PMC2662176: complete cached Experimental Procedures and Results were read. Human alpha2 and human beta1 were expressed in Xenopus oocytes. The construct called WT carries Q116R/N127D to allow pharmacological discrimination from endogenous pumps. Measurements include two-electrode voltage-clamp currents, rubidium uptake and membrane-protein detection. These are direct human-protein measurements in a nonhuman host, not purified reconstituted flux or unmodified-human-sequence controls. Mutation-dependent targeting, affinity and conformational defects support the central pump mechanism. Figure images and individual supplementary tables were not inspected.
PMID20100892, original PMC2812498: complete Methods and selected full Results paragraphs on outward pump current, Na/K-free currents, acidification and carboxy-terminal mutants were read, with selected Discussion. Human alpha2/beta1 was expressed in Xenopus oocytes; the reference alpha2 again uses Q116R/N127D. Under sodium/potassium-free acidic conditions, the reference pump exhibits an inward proton component. The deletion mutant also exhibits substantial sodium leak. This supports row 116 as a conditional non-core transport mode, not obligatory H+ transport stoichiometry or a normal human proton-pump core. Full Results outside those selected sections and all image pixels remain unread.
PMID18052210: the complete normal abstract identifies active human alpha2 paired with porcine beta1, expressed in Pichia and purified in detergent with lipid/FXYD1 stabilization. The mixed-species partner and preparation type must remain explicit. PMID10636900 describes functional combinations of human alpha and beta isoforms in Xenopus. PMID23954377 reports variant effects on function, alpha/beta interfaces and apparent ion affinities. Their complete abstracts were read; no claim is made to complete Methods in those three papers. Clearly established pump, ATP/ion-binding and complex terms can be retained by curator deference plus the independent direct studies.
PMID19683723, original PMC2749246: the complete de-duplicated cached Methods, Results and Discussion were read. This mouse cardiac beta1 deletion study measures alpha isoforms rather than merely mentioning a different gene: alpha1 decreases, alpha2 abundance does not significantly change, and ATPase activity, calcium handling and contractility are affected. It does not measure current passage between adjacent cytoplasms through intercellular protein channels. The official GO0086064 definition requires that intercellular-current mechanism. Row 113 therefore overstates what the study demonstrates; this is not a title-based misattribution diagnosis.
PMID23608603, original PMC3720717: complete sections 1.3 and 2.3, with their displayed figure context, were read from the normal XML record. This is a review, not a new alpha2 experiment. It distinguishes outward, repolarizing pump current from depolarizing sodium-channel/NCX current and discusses alpha2 localization/calcium coupling. The official GO0086012 definition and parents concern the actual depolarizing phase. Row 112 is therefore over-annotated as a direct process assignment, while direction-neutral contraction regulation and the existing repolarization context can remain. Row 55 is retained as non-core review-supported calcium-release regulation, not direct calcium translocation by ATP1A2.
The original YAML WITH/FROM fields identify mouse alpha2 Q6PIE5, mouse alpha1 Q8VDN2 and rat alpha2 P06686. Official MGI/UniProt/Reactome identity observations distinguish these donors. In particular, phosphatase row 62 and positive-contraction row 94 use mouse alpha1. Earlier primary reading of the alpha1 phosphomonoesterase-loop study supports an empirical pNPP-hydrolysis claim for a mouse alpha1 fragment, but does not resolve conservation in alpha2. ATP hydrolysis alone is not phosphoric-monoester hydrolysis. Row 62 remains UNDECIDED rather than being dismissed because the protein is an ATPase.
PMID12805306, original PMC6740785: the complete official abstract, Introduction and the displayed early mouse-generation Methods were read; later access challenged. The abstract supports mouse alpha2 effects on glutamate/GABA uptake, fear/anxiety and amygdala/piriform cortical pathology. These support non-core neural/developmental transfers without making alpha2 a neurotransmitter transporter. PMID15564586: the complete official abstract and first two captions support embryonic mouse respiratory-network/chloride regulation. No complete-paper or human physiological experiment is claimed. The auditory, nicotine and mechanical-stimulus donor assays remain unresolved. Exploration and locomotion were subsequently assessed from the recovered complete main text, as recorded below; they are not inferred merely from general neurological relevance.
PMID30280653: the separately preserved richer staged HTML record's complete endothelial-ion-transport subsection was read. It describes abluminal Na/K-ATPase at family level; the passage does not resolve alpha2. The official GO0150104 definition concerns transport through the barrier. Row 115 remains UNDECIDED; the reading does not establish that the entire paper excludes ATP1A2. PMID24769233 has a complete cached proteomics abstract, but its exact ATP1A2 target table remains unverified, preserving uncertainty for row 122.
Ouabain's official ChEBI472805 entry classifies it as a steroid hormone. Consequently the steroid/steroid-hormone binding rows are not rejected on chemical nomenclature. They remain non-core inhibitor-binding/response properties. Human beta1 P05026 is the explicit generic-binding partner; beta1/beta2/beta3 are the three chaperone-binding partners in rows 97–99. The beta-subunit folding/assembly role does not mean alpha2 itself is a protein-folding chaperone.
Recommend one core: GO0005391, sodium/potassium-exchanging transporter activity, in GO0005890, at the plasma membrane. The existing sodium-export, potassium-import and electrochemical-gradient processes describe the work performed by the pump. No NEW annotations, speculative family IDs or additional proton/phosphatase/signaling cores are proposed. There was no P50993/ATP1A2 hit in the local GO-CAM index; this is not proof of global model absence. PAINT trees were not reconstructed, and target self-WITH/FROM is not circular evidence.
The prospective row map preserves all 127 source objects. It distinguishes validated-stage reading, canonical source availability, actual full-body sections, complete abstracts and unavailable target tables. No normal source or provider retry was used to manufacture missing evidence. The source import receipt and separate cache check close reproducibility; root review and the final independent recovered-source check passed before canonical authorship.
Root review, 2026-09-29. No canonical source cache is altered by these notes.
The original PMID14742675 paper was read for complete Methods, initial Results and figure captions. Human alpha1/alpha2 constructs and human beta1 were expressed in Xenopus; the binding measurements use prepared microsomes. That endpoint establishes ligand binding, not by itself a cellular response. Complete Discussion, figure pixels and supplements were not inspected. The normal cache remains abstract-only.
The original PMID10636900 paper supplies distinct functional evidence. The pump-current Methods and corresponding voltage-dependence Results and Figure 6 caption were inspected. Intact oocytes expressing human alpha1/beta1, alpha2/beta1 or alpha3/beta1 were tested before and after 100 micromolar ouabain; endogenous currents measured in uninjected oocytes were subtracted. These experiments measure a cellular electrical activity endpoint for human alpha2, beyond ligand binding. This is human-protein evidence in a Xenopus host. Only selected original sections and captions were read, not every Method/Result section, figures or supplements. The normal cache remains abstract-only; the additional source observation is preserved separately.
Official AmiGO definitions for GO:0071383 and GO:1903416 require a change in cellular activity/state, or cellular/organism activity/state respectively. The current endpoint supplies that distinction. ChEBI's previously verified steroid-hormone classification of ouabain is retained.
Root interpretation: retain the five existing response annotations as KEEP_AS_NON_CORE, with PMID10636900 explicitly linked as independent functional corroboration. Do not change their original evidence codes or sources, portray the microsomal assay as a cellular assay, or infer a new endocrine-signaling core. Row111 says TAS; row120's supplied sources are rat/mouse alpha2 and Ensembl, without ARBA. An independent finite check of this interpretation passed without required biological changes.
Normal donor publication fetch for PMID12805306 and PMID15564586 failed once with DNS resolution errors. Their web reading remains separately documented. The verified Source70 import recovered both normal records before final authorship; their exact titles and availability flags now appear in the reference list. PMID12805306 has additional HTML article text; PMID15564586 remains abstract-only. Complete canonical frontmatter and abstracts were read. No missing cache was invented.
Initial root draft status (before recovered-source behavior update): all 127 source objects and absent products preserved; {'KEEP_AS_NON_CORE': 55, 'ACCEPT': 57, 'UNDECIDED': 13, 'MARK_AS_OVER_ANNOTATED': 2}. One coupled-pump core, seven bounded reference findings, no NEW annotations. Normal donor cache recovery and the initial independent scientific draft review are closed. The final independent check also passed for the three updated behavior rows and the two exact reference objects; the other 124 annotation reviews and the single core remain unchanged. The core lists the two direct transport processes; gradient maintenance is described in prose. Focused validation, rendering and history are recorded below after canonical application.
After verified Source70 import, the complete normal PMID12805306 main text was read, including Methods, Results and Discussion. Mouse heterozygotes differed in novel-environment exploration tests, while home-cage activity and rota-rod coordination were unchanged. Homozygous E18.5 embryos lacked spontaneous movement. Rows 79, 80 and 87 are retained as non-core with those boundaries, replacing uncertainty caused by previously unavailable assay text. The official GO:0035641 definition concerns movement in a novel environment; GO:0040011 concerns self-propelled movement. These existing mouse-derived annotations do not establish direct human behavioral experiments. Figure images, missing image captions and supplements were not inspected. PMID15564586 remains abstract-only. Final counts: 57 ACCEPT, 58 KEEP_AS_NON_CORE, 10 UNDECIDED and 2 MARK_AS_OVER_ANNOTATED; all 127 machine-sourced objects, absent products and one pump core are preserved.
Focused validation (just validate human ATP1A2) passed with one advisory for the non-core generic beta-subunit binding row. Its verified interaction context is retained under the action policy. HTML rendering passed. A matching history record was scaffolded with just new-history; its validation is recorded separately. No new repository-wide validation PASS is claimed. All 19 normal source records, raw UniProt/GOA files and provider-attempt evidence are preserved.
The existing IPI interaction with human beta1 (UniProtKB:P05026) is refined to GO:0046982 protein heterodimerization activity. The GO definition and parents identify this as a molecular-function subtype of protein dimerization, describing association with a nonidentical protein into a heterodimer. The complete PMID:23954377 abstract describes alpha2 G900R/E902K at the alpha/beta interface and likely impairment of that interaction. The partner accession comes from the unchanged GOA IPI assertion; the abstract does not independently map it or expose the interaction assay. The prior alpha2/beta1 functional-assembly evidence supplies biological context. This refines the existing binding row; it neither replaces molecular function with a complex term nor adds a duplicate NEW annotation.
The requested exact chemical relationship appears in the official ChEBI:472805 ouabain record, outgoing relations, rechecked on 2026-09-29:
CHEBI:472805 (ouabain) is_a CHEBI:26764 (steroid hormone).CHEBI:472805 is_a CHEBI:38092 (cardenolide glycoside).has_role CHEBI:38147 (cardiotonic drug) relation describes another aspect and does not replace either class assertion.Thus the two steroid-hormone-binding rows retain their non-core decisions. The steroid-binding and steroid-stimulus-response reasons now also name the explicit axiom. The classification is not an inference that every steroid is a hormone and does not establish endogenous endocrine physiology. The previously documented microsomal binding and intact-oocyte current experiments remain distinct evidence types; no new original-paper reading beyond the complete PMID:23954377 abstract is claimed in this follow-up.
The ATP-metabolism comment concerns the existing GO:0046034 row (the review comment named GO:0006200). It remains ACCEPT because alpha2 performs ATP hydrolysis as part of the core transport reaction, which the single GO:0005391 core already states. The distilled core need not duplicate all broad parent annotations. The two cardiac specificity cautions remain MARK_AS_OVER_ANNOTATED: this follow-up adds no evidence that would warrant escalating the conservative calls to REMOVE. Other physiological and unresolved donor-assay decisions are unchanged. The older notes remain an append-only record; this section provides the concise biological rationale for the current changes.
The independently reviewed follow-up passed focused validation (just validate human ATP1A2, 3fd1e7), rendering (f2c5c7), and validation of the new EDIT history record 2026-09-29T201203Z-codex-06c8e5.yaml (399a22). The single generic-binding advisory is resolved by the supported molecular-function refinement. No repository-wide validation result is inferred from these focused checks.