Ninjurin1, a target of p53, regulates p53 expression and p53-dependent cell survival, senescence, and radiation-induced mortality

摘要: The tumor suppressor protein p53 plays a crucial role in coordinating cellular processes, such as cell cycle arrest, apoptosis, and senescence. nerve injury-induced 1 (Ninjurin1, Ninj1) is homophilic adhesion molecule involved regeneration. Interestingly, Ninj1 found to be overexpressed human cancer, but its tumorigenesis not clear. Here, we that transcriptionally regulated by can induced DNA damage p53-dependent manner. We also knockout or knockdown of increases expression potentially through enhanced mRNA translation. In addition, deficiency suppresses proliferation enhances apoptosis premature senescence Consistent with this, mice heterozygous ninj1 are hypersensitive ionizing radiation-induced lethality, along increased thymus. Taken together, provided evidence target modulates translation senescence, proliferation, mortality vitro vivo. Thus, postulate membrane molecule, an ideal regulate activity via the p53-Ninj1 loop.