McMasters K M, Montes de Oca Luna R, Peña J R, Lozano G
Department of Surgical Oncology, University of Texas MD Anderson Cancer Center, Houston 77030, USA.
Oncogene. 1996 Oct 17;13(8):1731-6.
The mdm2 gene encodes a protein that is necessary for the negative regulation of p53 function in vivo. Deletion of the mdm2 gene in mice results in early embryonic death while concomitant mdm2 and p53 deletion results in viable offspring. The viability of these mice prompted us to ask if MDM2 had an important growth regulatory function independent of p53. We established mouse embryo fibroblasts null for both p53 and mdm2 and compared them with p53-null fibroblasts. The cells did not differ in their growth rates or their ability to bypass a G1 arrest. Both cell lines formed colonies efficiently when plated at low density and showed a similar degree of genetic instability. Thus, the analysis of several growth parameters indicated no difference between p53-null and p53/mdm2-null cell lines.
mdm2基因编码一种蛋白质，该蛋白质在体内对p53功能的负调控是必需的。小鼠中mdm2基因的缺失会导致胚胎早期死亡，而同时缺失mdm2和p53则会产生可存活的后代。这些小鼠的存活促使我们探究MDM2是否具有独立于p53的重要生长调节功能。我们建立了p53和mdm2均缺失的小鼠胚胎成纤维细胞，并将其与p53缺失的成纤维细胞进行比较。这些细胞在生长速率或绕过G1期阻滞的能力方面没有差异。当以低密度接种时，两种细胞系都能高效形成集落，并且显示出相似程度的遗传不稳定性。因此，对几个生长参数的分析表明，p53缺失和p53/mdm2双缺失的细胞系之间没有差异。
