The strongest direct evidence identifies the α chain as part of the structure assembled into fibrinogen and fibrin. Human-chain assembly intermediates are followed experimentally in PMID:8910396 (Figures 1–5), and the human structure in PMID:19296670 retains the α chain while revealing preparation heterogeneity. Patient afibrinogenemia in PMID:10891444 is important necessity evidence; it is not the sole basis for assigning molecular structural activity.
FGA also fits the scaffold/cofactor participation criterion for fibrinolysis. The actual αC-oligomer binding and plasmin-generation measurements in PMID:21806028 (Figures 5–8) distinguish active assembled material from weak soluble monomers. Human fibrin truncations in PMID:37082262 (Figure 5) reduce but do not abolish tPA-mediated activation. This is work by a template/cofactor, not protease activity. Structural experiments in the latter paper (Figures 1–4) also show altered fibrin assembly, with longer lag but higher final turbidity. The EM timing and scale-bar discrepancies limit quantitative interpretation and are retained in the full reference assessment.
The raw product identities are essential. Three source contexts refer to free fibrinopeptide A and three to mature α chain; two pairs collapse into single seeded rows. Free FPA is not automatically a complex subunit or clot-forming scaffold merely because its cleavage permits fibrin formation. The product table preserves each raw identifier and feature. The two natural splice records remain unchanged, and no experimental fragment is declared a new natural product.
Receptor-dependent cell responses require similar restraint. ICAM-1 binding, endothelial survival and ERK responses in PMID:9182580 and PMID:10903502 concern assembled fibrinogen and include γ-chain recognition. Rat vascular and endothelial experiments with human fibrinogen in PMID:15739255 and PMID:19193866 remain species- and preparation-bounded. The positive outcomes are retained as contextual biology, without assigning independent α-chain receptor, kinase, hormone or secretion-machinery functions.
The exact YWHAQ association permits a specific 14-3-3-binding refinement. Conversely, the K18 screen does not demonstrate filament binding, and FAM20C phosphate transfer does not independently demonstrate a binding function distinct from substrate recognition. Related BioPlex maps are not counted as independent replications. The source guide and source records give the methods and stable article/table locators.
Source access remains consequential. The original R16C, Magdeburg, heterotypic adhesion, trophoblast spreading and free-FPA inhibitory contexts were not all recovered operatively. Generic claims with identical independently measured support are distinguished from unresolved partner, product or sample-specific claims. The three unresolved proteomics target contexts remain uncertain despite positive FGA measurements elsewhere.
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