| First Author | Zhang M | Year | 2017 |
| Journal | FEBS Lett | Volume | 591 |
| Issue | 21 | Pages | 3670-3681 |
| PubMed ID | 28948615 | Mgi Jnum | J:258331 |
| Mgi Id | MGI:6117905 | Doi | 10.1002/1873-3468.12861 |
| Citation | Zhang M, et al. (2017) NDRG2 acts as a PERK co-factor to facilitate PERK branch and ERS-induced cell death. FEBS Lett 591(21):3670-3681 |
| abstractText | NDRG2, a newly identified tumor suppressor, is also responsive to various stresses, such as hypoxia and DNA damage. Here, we reported that in human hepatoma SK-Hep-1 and HepG2 cells, NDRG2 mRNA and protein levels were upregulated by different endoplasmic reticulum stress inducers including Tg, Tm, and DTT. Further, using NDRG2-overexpressing hepatoma cell lines and Ndrg2KO mice liver tissues, we found that, among the three branches of unfolded protein response signaling, NDRG2 facilitates protein kinase RNA-like ER kinase (PERK) pathway via interaction with PERK, enhancing its downstream ATF4 and CHOP. Functionally, NDRG2 promotes ERS-induced apoptosis partially through ATF4 or CHOP. Thus, NDRG2 is a novel ERS-responsive protein and acts as PERK co-factor to facilitate PERK branch, thereby contributing to ERS-induced apoptosis. |
