The clearest direct molecular evidence is the purified-fragment exchange assay in PMID:8969170, Figure 2. Human FGD1 residues 330–710 promote GDP release and nucleotide loading on modified Cdc42Hs. The accompanying small-GTPase pulldown establishes substrate recognition, while the fibroblast assays connect exchange to Cdc42-dependent actin responses. They do not show direct actin binding, GTP-hydrolysis catalysis, or FGD1 kinase activity. The retained actin, filopodium and small-GTPase-binding roles are distinguished from the central exchange mechanism.
The source uses mouse Swiss 3T3 and NIH 3T3 recipient cells, and Sf9-derived recombinant proteins. The engineered DH–PH fragment is not a natural splice product. The original Methods, Results, Discussion and figure captions were read externally; the normal publication cache remains unchanged and abstract-only. Figure pixels were not recovered.
PMID:7954831 supplies strong human genetic disease association in its verified abstract, but the operative full text remains unavailable. The specific organ-morphogenesis assertion remains uncertain rather than being rejected from incomplete evidence. The 1996 paper’s developmental discussion does not supply the missing organ experiment.
The genuine default-provider attempt produced no report. No cause was inferred from its uninspected private trace. Source-specific methods, article locators and limitations are recorded in the direct source guide; the source table links each owned context to the canonical review, and the product table preserves construct boundaries. No new quotations, source rows or product objects were added.