The genuine inherited Falcon report provides historical background; its earlier reconciliation does not supersede source-specific primary reassessment. Current source-directed changes are documented in notes.

Bone-forming capacity persists in some manipulated OI MSC clones, including clones targeted at the wild-type allele; the experiment is not a uniform correction or an alpha2-alone osteogenic-instruction assay.

Patient-cell alpha2 C-propeptide variants delay incorporation into type I procollagen heterotrimers, supporting intrinsic chain-association work rather than a distinct adaptor activity.

The review describes collagen as structural ECM molecules and distinguishes fibrillar assemblies; this is family synthesis, not a new target-specific tensile-force experiment.

The human skin collagen experiment supports MMP-12 recognition and cleavage of type I/III collagen, including an explicitly identified alpha2 cleavage site; it does not make collagen a protease regulator.

The fetal-murine screen abstract positively reports collagen–SMAD associations confirmed with translated collagen and GST-SMAD MH2. Exact alpha2 attribution is supplied separately by current MGI IPI records; the full alpha2 construct remains unrecovered.

Mouse Mesd rescues receptor maturation in Boca-depleted Drosophila S2 cells. This is conserved partner-class support, not a direct human MESD folding assay or evidence that collagen is its substrate.

The abstract reports EIF3F deubiquitinase activity. Separately read original Results Figure 3A specify human bacterial-coexpression constructs; murine probe/rescue experiments are distinct. This supports the partner class, not a collagen substrate or Notch role.

Reconstituted tail-anchored-client capture supports SGTA as a client-handling transport chaperone. Its isolated complex does not execute insertion or ubiquitination, and the study is not a COL1A2 interaction-specific negative control.