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Generation and Characterization of the Anp32e-Deficient Mouse

2010; Public Library of Science; Volume: 5; Issue: 10 Linguagem: Inglês

10.1371/journal.pone.0013597

1932-6203

Patrick T. Reilly, Samia Afzal, Andrew Wakeham, Jillian Haight, Annick You-Ten, Kathrin Zaugg, Joanna Dembowy, Ashley Young, Tak W. Mak,

Ubiquitin and proteasome pathways

Background Accumulated literature suggests that the acidic nuclear phosphoprotein 32 kilodalton (Anp32) proteins control multiple cellular activities through different molecular mechanisms. Like other Anp32 family members, Anp32e (a.k.a. Cpd1, PhapIII) has been conserved throughout vertebrate evolution, suggesting that it has an important function in organismal survival. Principal Findings Here, we demonstrate that the Anp32e gene can be deleted in mice without any apparent effect on their wellbeing. No defects in thymocyte apoptosis in response to various stresses, fibroblast growth, gross behaviour, physical ability, or pathogenesis were defined. Furthermore, combined deletion of Anp32a and Anp32e also resulted in a viable and apparently healthy mouse. Significance These results provide evidence that significant functional redundancy exists among Anp32 family members.