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. 2016 Jul 27;12(10):1776–1790. doi: 10.1080/15548627.2016.1199301

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Figure 6. — Atg5 is dispensable for nevi formation driven by oncogenic Braf^V600E in genetically modified mice. (A) Hyperproliferative pigmented lesions generated in the tamoxifen responsive Tyr::CreERT2;Braf^CA/CA mice crossed to Atg5^flox/flox animals for assessment of Atg5 gene dosage (Atg5^+/−, Atg5^+/Δ or atg5^Δ/Δ) in the melanocytic compartment. Shown are images of lesions generated in ears, paws or the back skin (the latter in insets) captured 6 mo after tamoxifen induction. Equivalent anatomical areas in tamoxifen-untreated (noninduced) Tyr::CreERT2;Braf^CA/CA;Atg5^+/− control animals are also included as a reference. (B) Visualization of ATG5 protein levels by immunohistochemical staining (pink) of paraffin-embedded ear sections of animals of the indicated genotypes and treated as in (A). Nuclei were counterstained by hematoxilin. The brown color corresponds to melanin.