The disqualification of Zmpste24 gene causes abnormalities in the architecture of the nucleus and causes multiple phenotypes associated with aging. The protein encoded by this gene is a metalloprotease that is involved in processing prelaminina A key component of the nuclear membrane.

The group of Dr. Lopez-Odin has developed mice deficient in Zmpste24, who has studied the molecular mechanisms underlying the phenotypic changes caused by a deficiency in this gene. The massive analysis of differentially expressed genes between wild and knockout mice, using the technology of DNA microarrays, revealed that mice deficient in Zmpste24presentaban proteins produced in response to clearly over expressed p53. The authors show directly the central role of p53 in aging processes associated with Zmpste24 deficiency by double-knockouts (Zmpste24-/ – and p53-/ -). The double-deficient mice with this phenotype have a more similar to wild-type mice, which only in Zmpste24-deficient animals.

The results presented here establish a direct relationship between the aging processes caused by abnormalities in the nuclear membrane and the tumor suppressor p53.The authors add that the development of mice deficient in components of the system-Zmpste24 lamininaA are a good model for studying aging in mammals.