Plays a role in the endoplasmic reticulum quality control (ERQC) system also called ER-associated degradation (ERAD) involved in ubiquitin-dependent degradation of misfolded endoplasmic reticulum proteins (PubMed:25066055, PubMed:24453213). Enhances SYVN1 stability (PubMed:24453213). Plays a role in LPL maturation and secretion (PubMed:25066055). Required for normal differentiation of the pancreas epithelium, and for normal exocrine function and survival of pancreatic cells (PubMed:20170518, PubMed:24453213). May play a role in Notch signaling (PubMed:20170518). Homodimer and homooligomer (PubMed:27064360). May form a complex with ERLEC1, HSPA5, OS9, and SYVN1 (By similarity). Interacts with FOXRED2 and EDEM1 (By similarity). Interacts with LPL and LMF1; may stabilize the complex formed by LPL and LMF1 and thereby promote the export of LPL dimers (PubMed:25066055). Component of the HRD1 complex, which comprises at least SYNV1/HRD1, DERL1/2, FAM8A1, HERPUD1/HERP, OS9, SEL1L and UBE2J1 (By similarity). SYNV1 assembles with SEL1L and FAM8A1 through its transmembrane domains, but interaction with its cytoplasmic domain is required to confer stability to FAM8A1 and enhance recruitment of HERPUD1 (By similarity). The interaction with SYNV1/HRD1 is direct (PubMed:25066055, PubMed:27064360). Highly expressed in pancreas, white adipose tissue, liver and spleen (at protein level) (PubMed:25066055, PubMed:24453213). Detected in heart, brain, spleen, lung, liver, kidney and testis (PubMed:9858735). First detected at 12.5 dpc in a small number of pancreas epithelial cells. Highly expressed in embryonic pancreas epithelium at later stages of embryonic development. N-glycosylated. Taxomifen-inducible gene disruption in adult mice leads to premature death within 3 weeks after the onset of taxomifen treatment. Mice progressively loose weight and become moribund despite increased food intake and normal blood glucose levels, suggesting nutrient maladsorption. After eight days of treatment, the pancreas was diffusely dark red and soft, suggesting severe pancreas atrophy. Still, the endocrine parts of the pancreas were not affected. Pancreas weight was about half of that of wild-type, the size of secretory zymogen granules was reduced and pancreatic lipase and alpha-amylase levels were strongly reduced. Besides, the morphology of the endoplasmic reticulum in pancreas acinar cells was abnormal, with swollen and fragmented cisternae. Likewise, SYVN1 protein levels are decreased, while those of other ERAD markers are increased (PubMed:24453213). Adipocyte-specific gene disruption does not give rise to any obvious phenotype when mice are kept on a low-fat diet. Mutant mice are resistant to diet-induced obesity when kept on a high-fat diet, in spite of normal food intake and physical activity. Mutant mice show dramatically reduced accumulation of fat mass relative to wild-type, while lean mass is not affected. Intriguingly, mutant mice display enlarged livers that develop steatosis and increased triglyceride levels. Mutant mice display increased fasting serum triglyceride and insulin levels. Likewise, mutant mice display hypertriglyceridemia after feeding, especially on a high-fat diet. In spite of increased cellular LPL levels, LPL secretion is reduced by 80 to 90% (PubMed:25066055). Gene disruption after residue 465 and replacement of the C-terminus with a beta-galactosidase-neomycin reporter gene construct leads to complete embryonic lethality; most die before 13.5 dpc. Only 5% of the embryos are viable at 15.5 dpc. Mutant embryos display defects in the differentiation of the pancreas epithelium. The defects in pancreas differentiation can be alleviated by pharmacological inhibition of Notch signaling (in vitro). Belongs to the sel-1 family.