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Recent Research Progress
Jagunal homolog 1 (JAGN1) takes part in the secretory pathway and is required for granulocyte colony-stimulating factor receptor–mediated signaling. JAGN1 emerges as a factor that is necessary in the differentiation and survival of neutrophils. In fact, JAGN1—encoding an ER-resident protein originally characterized in Drosophila melanogaster 16-was an attractive candidate. Some reports have Underlined that N-glycoprotein alteration results from faulty membrane trafficking due to the loss of JAGN1. Moreover, it has been reported that, JAGN1 interacts with a vesicular membrane trafficking complex known as Coat protein I (COPI). Furthermore, some findings imply that JAGN1 plays an important role in neutrophil survival. Mutations in the gene encoding JAGN1 was described as a novel disease-causing gene of severe congenital neutropenia (SCN), JAGN1-mutant neutrophils were characterized by abnormality in endoplasmic reticulum structure, absence of granules, abnormal N-glycosylation of proteins and susceptibility to apoptosis. Data published in several findings supported that the JAGN1 mutation is associated with SCN patients. Several reports show that two siblings with a homozygous mutation in JAGN1 gene, exhibiting multisystemic involvement.
The JAGN1 protein was identified in a SILAC proteomic screen of proteins that are increased in insulinoma cells expressing a folding-deficient proinsulin. JAGN1 mRNA was detected in primary rodent islets and in insulinoma cell lines and the levels were increased in response to ER stress. The function of JAGN1 was assessed in insulinoma cells by both knock-down and over-expression approaches. Knockdown of JAGN1 caused an increase in glucose-stimulated insulin secretion resulting from an increase in proinsulin biosynthesis. On the contrary, over-expression of JAGN1 in insulinoma cells resulted in reduced cellular proinsulin and insulin levels. JAGN1 can also regulate proinsulin biosynthesis in pancreatic β-cells. Therefore, under ER stress conditions JAGN1 is induced which might contribute to reducing proinsulin biosynthesis, in part by helping to relieve the protein folding load in the ER in an effort to restore ER homeostasis.