| First Author | Oh-hashi K | Year | 2009 |
| Journal | Biochem Biophys Res Commun | Volume | 387 |
| Issue | 3 | Pages | 504-10 |
| PubMed ID | 19615339 | Mgi Jnum | J:152541 |
| Mgi Id | MGI:4359106 | Doi | 10.1016/j.bbrc.2009.07.047 |
| Citation | Oh-hashi K, et al. (2009) CRELD2 is a novel endoplasmic reticulum stress-inducible gene. Biochem Biophys Res Commun 387(3):504-10 |
| abstractText | Recently, endoplasmic reticulum (ER) stress responses have been suggested to play important roles in maintaining various cellular functions and to underlie many tissue dysfunctions. In this study, we first identified cysteine-rich with EGF-like domains 2 (CRELD2) as an ER stress-inducible gene by analyzing a microarray analysis of thapsigargin (Tg)-inducible genes in Neuro2a cells. CRELD2 mRNA is also shown to be immediately induced by treatment with the ER stress-inducing reagents tunicamycin and brefeldin A. In the genomic sequence of the mouse CRELD2 promoter, we found a typical ER stress responsible element (ERSE), which is well conserved among various species. Using a luciferase reporter analyses, we demonstrated that the ERSE in mouse CRELD2 is functional and responds to Tg and ATF6-overexpression. Each mutation of ATF6- or NF-Y-binding sites in the ERSE of the mouse CRELD2 promoter dramatically decreased both the basal activity and responsiveness toward the ER stress stimuli. Our study suggests that CRELD2 could be a novel mediator in regulating the onset and progression of various ER stress-associated diseases. |
