FAM174C

FAM174C (C19orf24) encodes a non-classically secreted protein that reaches the extracellular space independently of the canonical ER-Golgi route: it lacks a signal peptide, its secretion is resistant to brefeldin A, and it fails to co-localize with the Golgi apparatus (PMID:16847563). The protein carries no N-glycosylation, and its expression is restricted to liver with preferential expression in normal over tumor tissue (PMID:16847563). Beyond these observations of unconventional secretion and tissue-restricted expression, no molecular activity, binding partner, or downstream pathway for FAM174C has been characterized in the available corpus.

1. 2006 Medium

   Whether FAM174C, a protein lacking a signal peptide, is retained intracellularly or exported was unknown; defining its trafficking route established it as a non-classically secreted protein bypassing the ER-Golgi pathway.

   Evidence Live-cell fluorescence imaging with a Golgi marker, brefeldin A inhibition assay, and PNGase F deglycosylation in HeLa cells

   PMID:16847563

   Open questions at the time

   • The molecular identity of the Golgi-independent secretion pathway is unknown
   • No secretion machinery or chaperone partner identified
   • Trafficking demonstrated in HeLa cells, not in the native liver context
2. 2006 Medium

   The post-translational modification status and tissue distribution were uncharacterized; showing absence of N-glycosylation and liver-restricted expression localized the protein's biological context.

   Evidence PNGase F deglycosylation assay and RT-PCR across multiple human tissues

   PMID:16847563

   Open questions at the time

   • Functional consequence of preferential normal-versus-tumor expression unknown
   • No protein-level confirmation of tissue distribution
   • Other potential post-translational modifications not assessed

• The molecular function, binding partners, and the identity of the unconventional secretion pathway used by FAM174C remain unknown.
• No molecular activity assigned
• No physical interaction partners identified
• The non-classical secretion route remains molecularly undefined