Molecules and Cells

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Fig. 1.

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Fig. 1. Runx3 inactivation, but not p53 inactivation, enables immediate proliferation of K-Ras–activated lung epithelial cells. (A and B) KPT and KRT mice were targeted with Ad-Cre (2.5 × 107 PFU/mouse, as described by DuPage et al., 2009), and Tomato-positive lung epithelial cells were assessed after 10 days. Clusters of Tomato-positive cells were detected 10 days after infection only in KRT mice lungs. Enlarged images of the boxed regions are shown (lower panels). (C) Schematic representation of the structures of K-RasLoxP-STOP-LoxP-G12D (K-Ras*), Runx3flox, p53flox, and Cretm/ERT1 (CreERT1) alleles. Cre recombinase activates K-Ras by removal of a knocked-in STOP transcriptional cassette from the K-RasLoxP-STOP-LoxP-G12D allele and inactivates the p53flox and Runx3flox alleles by deletion of exons. Survival curves of KR, R-CreERT1, K-CreERT1, KP-CreERT1, and KR-CreERT1 mice in the absence of tamoxifen are shown. The median survival of KR-CreERT1 mice was 48 days. No mice of other genotypes died within 50 weeks after birth (the duration of the experiment). (D) Hematoxylin/eosin (HE) staining of the lungs of K-CreERT1, KP-CreERT1, and R-CreERT1 mice (6 months after birth). A magnified image of the boxed region is shown on the right. Adenomatous lesions in a R-CreERT1 lung are indicated by dotted circles. HE staining of the lung tumors of KR-CreERT1 mice (2 and 8 weeks after birth).
Mol. Cells 2020;43:889~897
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