id: Pfam:PF11819
pfam_id: PF11819
name: Cytohesin Ubiquitin Protein Inducing Domain
short_name: CUPID
seed_status: EX_DUF
characterization_status: UNSCORED
curation_status: SEEDED
source_url: https://www.ebi.ac.uk/interpro/api/entry/pfam/PF11819
counters:
  proteins: 5709
  matches: 5767
  proteomes: 1147
  taxa: 3723
  structures: 0
  alphafold_models: 4876
  domain_architectures: 65
provenance:
  snapshot_id: interpro-pfam-duf-2026-10-10
  path: data/worklists/interpro-pfam-duf-2026-10-10.json
  sha256: 17fb625876c9326ed284263a47bcd84e0d7844a31c040dc06cd2260c36f1c383
  generated_at: '2026-10-10T07:44:21.614711Z'
  source_url: https://www.ebi.ac.uk/interpro/api/entry/pfam/
interpro_id: InterPro:IPR021774
description: 'C1ORF106 also known as INAVA (Innate Immune Activator), is identified as a risk factor for
  the chronic inflammatory bowel diseases (IBD). Mice lacking the protein show defects in intestinal barrier
  integrity at steady state and greater susceptibility to mucosal infection. INAVA carries CUPID (Cytohesin
  Ubiquitin Protein Inducing Domain). Three other human proteins contain CUPID: FRMD4A, FRMD4B, and CCDC120-
  proteins implicated in neurite outgrowth, and in human cancer, Alzheimer''s, celiac, and heart disease.
  All appear to bind the ARF-GEF (guanine nucleotide-exchange factors) cytohesin family members, such
  as proteins (ARF 1-4), which regulate cell membrane and F-actin dynamics. INAVA-CUPID binds cytohesin
  2 (also known as ARNO), targets the molecule to lateral membranes of epithelial monolayers, and enables
  ARNO to affect F-actin assembly that underlies cell-cell junctions and barrier function. In the case
  of inflammatory signalling, ARNO can coordinate CUPID function by binding and inhibiting CUPID activity
  of acting as an enhancer of TRAF6 dependent polyubiquitination. In other words, ARNO acts as a negative-regulator
  of inflammatory responses. In summary, INAVA-CUPID exhibits dual functions, coordinated directly by
  ARNO, that bridge epithelial barrier function with extracellular signals and inflammation [[cite:PUB00101049]].'