May function in the control of the neuroendocrine secretory pathway. Proposed be a specific endogenous inhibitor of PCSK1. ProSAAS and Big PEN-LEN, both containing the C-terminal inhibitory domain, but not the further processed peptides reduce PCSK1 activity in the endoplasmic reticulum and Golgi. It reduces the activity of the 84 kDa form but not the autocatalytically derived 66 kDa form of PCSK1. Subsequent processing of proSAAS may eliminate the inhibition. Slows down convertase-mediated processing of proopiomelanocortin and proenkephalin. May control the intracellular timing of PCSK1 rather than its total level of activity (By similarity).
Endogenous ligand for GPR171. Neuropeptide involved in the regulation of feeding.
Endogenous ligand for GPR171. Neuropeptide involved in the regulation of feeding.
Subcellular locations: Secreted, Golgi apparatus, Trans-Golgi network
A N-terminal processed peptide, probably Big SAAS or Little SAAS, is accumulated in cytoplasmic protein tau deposits in frontotemporal dementia and parkinsonism linked to chromosome 17 (Pick disease), Alzheimer disease and amyotrophic lateral sclerosis-parkinsonism/dementia complex 1 (Guam disease).
Expressed in brain and pancreas.