Mouse loss-of-function, rescue and microscopy connect CC2D2A to mother-centriole appendages, ciliary assembly and transition-zone elaboration. Loss disrupts cilia-dependent Shh signaling and embryonic laterality/neural development. These developmental roles arise through ciliary organization.
Horse N-terminal deletions align within the human predicted disordered1–241region, while the long coiled-coil/C2 architecture is retained. This supports broad ciliary/developmental transfer. Renal tubule ciliation defects alone do not resolve the more specific kidney-development claim, which remains UNC.
The reproducible alignment, source paths and hashes are in the paired comparison. Current UniProt sequences have not been proven identical to the original ProtNLM input sequences. Sequence anomalies are therefore recorded as model/transfer limitations, not as proven wrong-input pipeline errors.
Confirm the horse transcript model and distinguish renal morphogenesis from renal cilia/homeostasis. A calcium-binding molecular activity should not be invented solely from the C2 domain label.
Every seeded annotation receives a current assessment. UNDECIDED marks unresolved source-specific or biological evidence; these are initial reviews rather than a claim that every original experimental assay has been independently reproduced or verified. The human Edison report is retained as a research synthesis and source-finding aid; decisive YAML excerpts cite primary publications, source records or reproducible analysis. The validator advisory to cite the deep-research file is deliberately not satisfied by citing AI prose as biological proof.