Comment on: Torii et al. (2009) Gene Silencing of Phogrin Unveils Its Essential Role in Glucose-Responsive Pancreatic β-Cell Growth. Diabetes 58:682–692
- From the Experimental Medicine Section, Oral Infection and Immunity Branch, National Institutes of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland.
- Corresponding author: Abner L. Notkins, anotkins{at}mail.nih.gov.
In the March 2009 issue of Diabetes, Torii et al. (1) reported that neither the knockdown nor the overexpression in MIN6 cells of insulinoma-associated protein (IA)-2β (also known as phogrin), a transmembrane dense core vesicle (DCV) protein, had any effect on glucose-stimulated insulin secretion (GSIS). These findings, however, differ from those of Doi et al. (2), who reported that the overexpression of IA-2β in MIN6 cells inhibited GSIS, whereas the knockdown of IA-2β in MIN6 cells had little …
