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Experimental Medicine Section, Oral Infection and Immunity Branch (OIIB), National Institute of Dental and Craniofacial Research (NIDCR), The National Institutes of Health (NIH), Bethesda, Maryland 20892, USA
¹ Laboratory of Bioengineering and Physical Science, National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, Maryland 20892, USA
² Structure Biophysics Laboratory, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA
³ Department of Molecular, Microbial and Structural Biology, University of Connecticut Health Center, Farmington, Connecticut 06030, USA
⁴ Therapeutics Branch of NIDCR, NIH, Bethesda, Maryland 20892, USA

(Correspondence should be addressed to T Cai; Email: tcai{at}mail.nih.gov)

^* (G Zhang and H Hirai contributed equally to this work)

The regulated endocrine-specific protein, RESP18, first found in the rat pituitary, was thought to be regulated by dopaminergic drugs. Bioinformatics studies showed that RESP18 shares sequence homology with the luminal region of IA-2, a dense core vesicle (DCV) transmembrane protein involved in insulin secretion. The present study was initiated to examine the genomic structure and subcellular localization of RESP18 and the effect of glucose on its expression. Human RESP18 was isolated from a pancreas cDNA library and its subcellular localization was determined by immunoelectron microscopy. MIN6 cells and mouse islets were used to study the effect of glucose on RESP18 expression. Bioinformatics analysis revealed that RESP18 and IA-2 are tandemly arranged within a 45 kb region on human chromosome 2 and share common intron–exon boundaries. By confocal microscopy, RESP18 was found in , ß and cells in the pancreatic islets. Electron microscopy revealed that RESP18 is present in the lumen of DCVs. The expression of RESP18 in ß cells is markedly increased following exposure to high glucose and also elevated in the islets of diabetic, but not non-diabetic, NOD mice. We conclude that RESP18 is a luminal protein of DCVs and its expression is regulated by exposure to glucose.