Gene Ontology annotation through association of InterPro records with GO terms

Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity

GO_REF:0000033

Annotation inferences using phylogenetic trees

GO_REF:0000044

Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt

GO_REF:0000052

Gene Ontology annotation based on curation of immunofluorescence data

PMID:25416956

A proteome-scale map of the human interactome network.

PMID:28041644

Mutations in PIH1D3 Cause X-Linked Primary Ciliary Dyskinesia with Outer and Inner Dynein Arm Defects.

Human disease-associated DNAAF6 deficiency disrupts outer and inner dynein-arm assembly; sequence-confirmed human constructs support DNAAF2/DNAAF4 association, with HSP90 tested as fragments.

PMID:28176794

X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3.

Human tagged DNAAF6 and DNAI2 associate with swapped tags and controls; a missense variant and three truncating variants lose the co-IP signal. Human airway imaging supports TGN enrichment, and residual dynein arms and motility vary among affected individuals.

PMID:32296183

A reference map of the human binary protein interactome.

PMID:24421334

Pih1d3 is required for cytoplasmic preassembly of axonemal dynein in mouse sperm.

PMID:9488487

Cloning and biochemical characterization of TAF-172, a human homolog of yeast Mot1.

file:human/DNAAF6/DNAAF6-evidence-guide.md

DNAAF6 source and evidence guide

PMID:30354218

NOX4 (NADPH Oxidase 4) and Poldip2 (Polymerase δ-Interacting Protein 2) Induce Filamentous Actin Oxidation and Promote Its Interaction With Vinculin During Integrin-Mediated Cell Adhesion.

Human aortic smooth-muscle POLDIP2 knockdown reduces actin–vinculin association and focal-adhesion maturation. The actin–vinculin response to POLDIP2 overexpression depends on NOX4, supporting an upstream cytoskeletal-regulatory role rather than demonstrated direct actin crosslinking. This is partner-class evidence, not a DNAAF6-dependent process.