| First Author | Ozaki N | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 446 |
| Issue | 1 | Pages | 224-30 |
| PubMed ID | 24607897 | Mgi Jnum | J:219129 |
| Mgi Id | MGI:5619688 | Doi | 10.1016/j.bbrc.2014.02.111 |
| Citation | Ozaki N, et al. (2014) Autophagy regulation in pancreatic acinar cells is independent of epidermal growth factor receptor signaling. Biochem Biophys Res Commun 446(1):224-30 |
| abstractText | Autophagy is an intracellular degradation system in eukaryotic cells that occurs at a basal level. It can also be induced in response to environmental signals including nutrients, hormones, microbial pathogens, and growth factors, although the mechanism is not known in detail. We previously demonstrated that excessive autophagy is induced within pancreatic acinar cells deficient in Spink3, which is a trypsin inhibitor. SPINK1, the human homolog of murine Spink3, has structural similarity to epidermal growth factor (EGF), and can bind and stimulate the EGF receptor (EGFR). To analyze the role of the EGFR in pancreatic development, in the regulation of autophagy in pancreatic acinar cells, and in cerulein-induced pancreatitis, we generated and examined acinar cell-specific Egfr-deficient (Egfr(-/-)) mice. Egfr(-/-) mice showed no abnormalities in pancreatic development, induction of autophagy, or cerulein-induced pancreatitis, suggesting that Egfr is dispensable for autophagy regulation in pancreatic acinar cells. |
