Generation and characterization of the Anp32e-deficient mouse.
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.


RESULTS
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.


CONCLUSIONS
These results provide evidence that significant functional redundancy exists among Anp32 family members.
Department of Cellular and Molecular Research, National Cancer Centre Singapore, Singapore, Singapore.
Patrick T
PT
Reilly
Samia
S
Afzal
Andrew
A
Wakeham
Jillian
J
Haight
Annick
A
You-Ten
Kathrin
K
Zaugg
Joanna
J
Dembowy
Ashley
A
Young
Tak W
TW
Mak
D000818:Animals; D018797:Cell Cycle Proteins / Q000235:genetics*; D051379:Mice; D008810:Mice, Inbred C57BL; D009419:Nerve Tissue Proteins / Q000235:genetics*; D009687:Nuclear Proteins / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction
C485862:Anp32b protein, mouse; D018797:Cell Cycle Proteins; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins