Source: pre-release post-processed-2026_02_28k.xml, accession O14003. The exact entry is preserved in rfc3-protnlm-source.xml; all original evidence elements and model scores are retained in rfc3-protnlm-source.json. This record is currently Swiss-Prot and is absent from the published 26,856-record TrEMBL pilot list. The current public ProtNLM endpoint returns this record; API availability is distinct from membership in the published pilot list. No training-membership inference is made.
May be involved in DNA replication and thus regulate cell proliferation.
Original evidence key(s): 2.
| Atomic claim | Assessment | Evidence and limit |
|---|---|---|
| Participation in DNA replication | CNN | Target rfc3-1 mutants show DNA-replication defects (PMID:10588638), and RFC supports processive Pol delta synthesis (PMID:10748208). The cautious phrase “May be” understates the established process role. |
| Consequent regulation of cell proliferation | CNN | The same target study establishes an essential growth role and defects in replication and damage checkpoints. Interpreted as coupling proliferation to successful genome replication, the statement is supported; it does not identify Rfc3 as an independent mitogenic signaling factor. |
publications/PMID_10588638.md).publications/PMID_10748208.md).publications/PMID_16040599.md).Family and feature provenance: rfc3-uniprot.txt.