This review covers 66 current human P14867 contexts. It records 47 ACCEPT, 5 KEEP_AS_NON_CORE, 11 MODIFY and 3 UNDECIDED decisions, with no NEW annotation. The original 66 raw objects and all native machine fields remain unchanged. A genuine seeded fetch produced the same 66 contexts and all 16 export columns as the retained forecast. The source evidence records the actual joins and the three restored extension atoms. Scoped-check outcomes are reported in the notes.
GABRA1 encodes the 456-residue alpha1 precursor. UniProt records signal-peptide processing at residues 1–27 and a mature chain spanning 28–456, with no declared alternative protein products. A historical partial cDNA, pathogenic truncations, engineered loop replacements, tags, preparation proteolysis and the ELIC/alpha1 chimera do not establish additional natural products.
Human alpha1 contributes a complementary GABA-recognition interface with beta subunits and transmembrane pore structure to GABA-A heteropentamers. The core records contribution to GABA-gated chloride channel activity, GABAergic synaptic transmission and chloride transmembrane transport, at plasma/postsynaptic membranes in the GABA-A complex. No independent alpha1 homopentamer or invented subunit-specific molecular function is asserted. Ionic gradients determine the direction and electrical effect of chloride movement.
The direct human functional evidence includes PMID2465923, PMID29950725 and PMID30602789. The first was read as an authentic abstract; selected original Methods, Results and captions were read for the latter two. The 2018 structure uses engineered loops. The 2019 full-length tagged preparation includes minor alpha1 proteolysis, and the uncertain pocket density plus GABA docking does not independently identify bound GABA. Neither a closed/desensitized structure nor artificial loops negate actual receptor current measurements.
Composition matters. Native mouse alpha1/delta evidence in PMID17159992 was read at abstract scope. PMID18204487 supplies oocyte alpha1/beta2/delta functional evidence, with abstract and selected public-caption access but unavailable full text. Human alpha1/beta3 constructs and wild-type comparisons in PMID35140402 were read in selected original sections. These support a composition-dependent extrasynaptic context, kept non-core, without assigning every alpha1 receptor to an extrasynaptic pool.
The original co-culture studies PMID23909897 and PMID25489750 provide receptor-dependent contacts and functional postsynaptic currents in rat-neuron/HEK preparations. Their assembly contribution is retained as non-core. Host species does not establish the origin of every cDNA. JoVE Figure 2 reuses earlier data, and its Figure 1B caption repeats beta2 despite the beta3 context. These limitations remain explicit; no image or raw electrophysiology data was independently inspected, and no unique alpha1 adhesion site is inferred.
The ELIC extracellular/human alpha1 transmembrane chimera in PMID30266951 was examined in the retained original publisher text. Propylamine/steroid responses and engineered pentamers do not alone establish native alpha1 orthosteric recognition or physiological homopentamers. The existing complex annotation remains biologically supported by independent human heteromer studies and the authentic abstract of PMID39843743, which reports native alpha1-containing complexes from epilepsy patients. The initial reading for that 2025 study was abstract-only. After genuine native acquisition, selected Methods, Results and Discussion were read independently. Anti-alpha1 purification of pooled epilepsy-surgery tissue supports native human alpha1/beta2 and alpha1/beta3 assemblies, with five maps containing unresolved subunit mixtures. Preparation abundance is not generalized to healthy tissue, and tentative accessory-partner assignments are not asserted as specific direct interactions. Figure images, raw maps and the complete mass-spectrometry table were not inspected.
The 11 MODIFY decisions retain positive evidence and refine broad terms to already asserted receptor, channel, chloride-transmembrane, plasma-membrane or GABA-A-complex terms. Official QuickGO definitions and typed paths were retained for all 28 incoming terms and the proposed relationships. The postsynaptic-membrane relation to postsynapse is explicitly part_of, not is_a. The contextual postsynaptic-potential molecular activity is retained; a GABA-specific child is not invented. The general GABA signaling process is retained because both synaptic and extrasynaptic settings are supported, rather than narrowing the whole claim exclusively to the extrasynaptic child.
Raw 42 remains UNDECIDED: PMID25025157 does assay alpha1 surface expression, but the selected spine passage concerns PSD95 and the precise alpha1 spine-localization panel is unresolved. This is not a wrong-gene conclusion from a gephyrin-focused title. Raw 52/53 remain UNDECIDED for the specific cytoplasmic-vesicle membrane assertion. The current rat donor has a same-term SL-derived electronic row. The rat UniProt P62813 record has now been inspected and links this location to PMID25172774 with ECO:0000269. The authentic abstract describes gamma2-containing receptor transport and KIF21B perturbation. Full text was not recovered, so no alpha1-specific panel, construct or vesicle population is claimed. The two alpha1 judgments remain UNDECIDED; the identified experimental source does not establish circularity or refute localization. PMID25172774 is explicitly included and was acquired missing-only after bounded ownership qualification; its native cache remains abstract-only.
Rat, mouse and bovine donor records were read as official GOA data. Their literal identifiers, evidence, references and extensions are retained separately from human target evidence. Donor PMID records are not marked independently read merely because their identifiers occur in those responses. The bovine postsynaptic-membrane claim has limited current donor detail but independent target-context support, so it is retained. The HPA method was read; no particular target image or antibody was inspected.
Actual PTHR18945 book/tree/alignment and literal IBD records place P14867 at AN1963/PTN002498429. All eight incoming IBA assertions descend to the target, with no retained target-path loss. Seven originate at PTN008360627; plasma-membrane raw 40 originates at PTN001054635. Raw 40's incoming 66 donors dated 20260529 are an older subset of the retained 147 donors dated 20260828. Both versions remain unchanged. Target self-donation is legitimate experimental grounding, and donor count is not an evidentiary score. The ungapped target sequence exactly matches the canonical 456 residues. No canonical family file was altered.
Reactome975340 resolves its catalyst through heteropentamer and GABRA sets to entity 975262, human P14867 residues 28–456 at plasma membrane. Reactome977443 directly includes that event. Reactome1236394 includes event 9612639 and a GABRA1-containing input, but that event is explicitly inferred and the endocytosis mechanism remains unresolved. These are exact model memberships, not direct human experimental verification of every branch, and do not give alpha1 ERBB4 kinase activity or create a new process assertion.
The 36 manual assessments cover 23 authentic PubMed abstracts, nine official GO_REF methods, three Reactome records and current UniProt. Selected original sections supplement the abstracts for eight papers; complete article reading, supplementary-image inspection and raw-data analysis are not claimed. The accompanying reference-access ledger distinguishes each paper's precise scope and retains its public URL. Official GO_REF descriptions were read from the retained complete gorefs.yaml; failed 404 stubs were excluded. Individual ARBA rule conditions were not comprehensively audited.
The actual normal-source union contains 29 paths: 23 publications, three Reactome entries and three existing family files. At accepted base 3c6145f, six sources were present and 23 absent; the relevant source and alias paths were unchanged at the later observed main 6f768239. Missing-only native acquisition added 21 publications and two Reactome records. All six existing source bytes remain exact. Nine publication caches contain full text, including newly available PMID28978485 and PMID39843743. Only the explicitly selected PMID39843743 sections expanded the manual reading scope; no new reading is claimed for PMID28978485. Failed full-text attempts for PMID18204487 and PMID24623842 are recorded as abstract-only. The original 13-word core quotation remains exact. The follow-up adds nine short primary-source anchors at selected direct-evidence and refinement judgments; reference-only reuse avoids repeated quotation beyond the per-paper budget. Exact cache offsets and occurrence counts are recorded in the source evidence. No pre-existing GABRA1 review, notes or quote archive was found in the bounded namespace checks.
Original raw 0/1/2 contributes_to qualifiers remain intact. Raw 6's conjunction preserves part_of GO:0051932, has_input CHEBI:17996 and has_output CHEBI:17996. The native parser omitted this conjunction; all three atoms are restored literally at native row 1 using the verified BFO/RO predicates and GO/ChEBI terms. The raw conjunction and untouched parser object are retained separately. This restoration is source metadata, not a new biological assertion. Genuine CREATE history and scoped-check outcomes accompany the canonical review.
The retained official QuickGO response records GO:0160001 extrasynaptic signaling via GABA as an is_a child of GO:0007214 gamma-aminobutyric acid signaling pathway. GO:0007214 is defined by GABA binding and the resulting receptor signals. GO:0051932 additionally encompasses vesicular release and the postsynaptic response; a name resemblance is not used as proof of an is_a edge. The whole GABA-signaling claim is retained because alpha1 supports synaptic as well as composition-dependent extrasynaptic receptor signaling. The eleven refinement paths remain unchanged.
The updated reasons lead with the biological evidence; literal donor dates, raw/native index joins and restoration details remain in this guide and the source evidence. The latter retains all 66 original raw contexts, exporter joins and source identities for reproducibility. Its size is not additional biological evidence and its raw fields are not curation assertions. No current or historical source object is discarded to reduce line count.
The notes now include a biological synthesis and selected exact excerpts. Nine added anchors are distributed across six primary papers. Repeated quotation occurrences in review plus notes are counted together, with no paper exceeding 25 newly quoted words. The original core quote is unchanged; the new offset/hash ledger does not repeat the quotations. The remaining citations reuse those sources by reference rather than adding redundant excerpts. Existing background/variant reference assessments remain useful to the disease and product context even when not attached to an annotation; none is given an artificial citation merely to silence an advisory.
The ten accepted molecular-function contexts that retain the source relation enables concern alpha1 function within an assembled receptor. Alpha1 supplies part of the ligand-recognition interface and the shared transmembrane pore; the functional evidence is from alpha1-containing receptor preparations, not isolated alpha1 channels. ACCEPT retains that supported molecular role. It does not establish autonomous activity of an isolated subunit.
The official GO annotation guidance distinguishes a function executed by a gene product from a complex function that cannot be ascribed to an individual subunit. It does not define enables simply as activity measured in isolation. Because alpha1 makes identified ligand-contact and pore-forming contributions, the source relations are preserved without declaring them verified upstream errors solely from heteropentamer assembly. The authored core uses contributes_to_molecular_function and in_complex to make the assembly context explicit. Existing contributes_to source rows retain that more explicit relation. This is an interpretation of the reviewed receptor function, not a source-file correction or a claim that all complex subunits should receive enables.
The contextual GO:1904315 assertions also retain their source relations and current ACCEPT decisions. Their postsynaptic-potential context remains explicit; the optional precomposition project suggestion does not change these source assertions in this bounded follow-up. All 66 actions, source fields, extensions, reference assessments, products, cores and quotations are unchanged.