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. Author manuscript; available in PMC: 2014 Jul 9.
Published in final edited form as: Cell Rep. 2014 Feb 20;6(5):844–854. doi: 10.1016/j.celrep.2014.01.030

Figure 1. Knock-in of C-terminal truncated Pten reduces mouse lifespan due to spontaneous tumor development.

Figure 1

(A) Schematic diagram of strategy for knock-in of the Pten point mutation, c.565A>T, leading to deletion of the Pten C-terminal domain (aa189-403). (B) Confirmation of the point mutation of c.565A>T by direct sequencing of Pten exon 6 in Pten+/+ and Pten+/ΔC ES clones. (C) The expression of the C-terminal truncated PtenΔC in various tissues of Pten+/ΔC mice examined by immunoprecipitation with an N-terminus-specific PTEN antibody prior to FLAG immunoblotting. Corresponding tissues from wild-type mice were included as controls. (D) Kaplan-Meier plot for overall survival of Pten+/+ and Pten+/ΔC mice. (E) Kaplan-Meier plot showing significantly shorter latency of tumor development in Pten+/ΔC mice as compared with wild-type control mice. (F) Incidence of tumor in different tissues. Pten+/ΔC mice aged from 12 to 60 weeks (n=35, 14 males and 21 females) were subjected to extensive histological evaluation. Enlarged lymph nodes were found in every mouse analyzed. Pheochromocytoma occurred in all Pten+/ΔC mice older than six months with a 12% frequency of pulmonary metastasis. See also Figure S1.