| First Author | Dong H | Year | 2021 |
| Journal | Oncol Rep | Volume | 45 |
| Issue | 2 | Pages | 595-605 |
| PubMed ID | 33416158 | Mgi Jnum | J:324584 |
| Mgi Id | MGI:7280813 | Doi | 10.3892/or.2020.7884 |
| Citation | Dong H, et al. (2021) Genetic deletion of Rnd3 suppresses apoptosis through NFkappaB signaling in the brain. Oncol Rep 45(2):595-605 |
| abstractText | Rho family GTPase 3 (RND3) is involved in multiple physiological activities involving the Rho kinasedependent signaling pathway. The present study revealed a novel role of RND3 in the regulation of apoptosis in the brain. Using immunofluorescence and TUNEL assays, a decreased rate of brain apoptosis was observed in Rnd3knockout mice. In addition, the function of RND3 in promoting apoptosis was determined in PC12 cells by immunoblotting assays and flow cytometry analysis in RNA interference and overexpression experiments. Furthermore, the present study demonstrated that Rnd3 and P65 protein interacted using immunoprecipitation analysis, and Rnd3 regulated apoptosis via its association with NFkappaB P65. Notably, Rnd3 blocked the antiapoptotic action of NFkappaB P65 in vitro by downregulating P65. Therefore, RND3NFkappaB P65 represents a novel signaling pathway in the regulation of brain apoptosis. The present study suggested an alternative approach for the treatment of neurodegenerative diseases through regulation of apoptosis via the RND3NFkappaB P65 signaling pathway in the central nervous system. |
