Extended Data Fig. 4: p38δ partially compensates for the lack of p38γ.

a, Kaplan–Meier analysis of survival in PHx-treated AlbCre and AlbCre-p38γ mice. n = 20 mice per genotype. Mantel–Cox log-rank tests were used. b, Rb phosphorylation in the liver was studied in AlbCre and AlbCre-p38γ mice by western blotting with the indicated antibody 48 h, 60 h and 72 h after PHx; each lane corresponds to a different mouse. The data are representative of at least three independent experiments. c, p38δ expression was studied by qPCR at different time points after PHx and its change in expression was represented. AlbCre mice: n = 7 and AlbCre-p38γ mice: n = 6. Comparisons were performed using a two-sided Student’s t-test. d–h, AlbCre control mice and AlbCre-p38γδ mice were subjected to 70% PHx or a sham procedure and were analysed after 48 h, 60 h or 72 h. d, Kaplan–Meier analysis of survival. A Mantel–Cox log-rank test was used. e, Immunoblot analysis of liver extracts from AlbCre-p38γδ mice with antibodies against phospho-Rb S807/S811, Rb, p38γ and vinculin (loading control); each lane corresponds to a different mouse. The data are representative of at least three independent experiments. f, g, Hepatocyte proliferation was analysed by BrdU incorporation (f; two-sided Student’s t-test; **P < 0.05) and Ki67 immunostaining (g; two-sided Student’s t-test with Welch’s correction; *P < 0.01) 48 h after PHx in AlbCre-p38γ (n = 3) and AlbCre-p38γδ (n = 3) mice. h, Hepatocyte proliferation was analysed by BrdU incorporation 60 h and 72 h after PHx in AlbCre mice (60 h, n = 9; 72 h, n = 7), AlbCre-p38γ mice (60 h and 72 h, n = 6) and AlbCre-p38γδ mice (60 h and 72 h, n = 3). Comparisons were performed using a one-way ANOVA coupled to Bonferroni’s post-tests; ***P < 0.001. Left, representative images. Scale bar, 50 μm. Right, quantification of Ki67- and BrdU-positive cells. Data are mean ± s.e.m. n = 5 counted areas from the specified number of mice.

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