Priority Research Perspective:
Sexually dimorphic tumor suppression by small mitochondrial Arf
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Jolieke G. van Oosterwijk1,3, Heather Tillman2 and Charles J. Sherr1,3
1 Department of Tumor Cell Biology, St. Jude Children’s Research Hospital, Memphis, TN, USA
2 Department of Pathology, St. Jude Children’s Research Hospital, Memphis, TN, USA
3 Howard Hughes Medical Institute, St. Jude Children’s Research Hospital, Memphis, TN, USA
Charles J. Sherr, email: firstname.lastname@example.org
Keywords: Arf tumor suppressor; small mitochondrial Arf (smArf); smArf sexual dimorphism
Received: January 02, 2019 Accepted: January 21, 2019 Published: February 08, 2019
Internal translational initiation of the mRNA encoding the Arf tumor suppressor yields an N-terminally truncated small Arf protein (smArf) that lacks amino acid residues required for Mdm2 binding and p53 activation. Here, we report that female, but not male, mice engineered to produce only smArf in lieu of the full-length Arf protein retain residual, sexually dimorphic tumor suppressive activity.
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