The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent concentration. Predicted molecular weight: 27 kDa.
Use a concentration of 3 µg/ml. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.
Use a concentration of 10 µg/ml.
FunctionMay 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. The function of the processed secreted peptides is not known.
Tissue specificityExpressed in brain and pancreas.
DomainProSAAS(1-180) increases secretion of enzymatically inactive PCSK1. The C-terminal inhibitory domain is involved in inhibtion of PCSK1. It corresponds to the probable processing intermediate Big PEN-LEN, binds to PCSK1 in vitro and contains the hexapeptide L-L-R-V-K-R, which, as a synthetic peptide, is sufficient for PCSK1 inhibition.
Post-translational modificationsProteolytically cleaved in the Golgi. O-glycosylated with a core 1 or possibly core 8 glycan.
Cellular localizationSecreted. 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.