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. Author manuscript; available in PMC: 2013 Nov 1.
Published in final edited form as: Nat Neurosci. 2013 Mar 31;16(5):532–542. doi: 10.1038/nn.3365

Figure 4. Inactivation of p53 rescues the defects of FIP200-null NSCs in vitro.

Figure 4

(A) Lysates are extracted from neurospheres of Ctrl, FIP200hGFAP cKO, p53hGFAP cKO, 2cKO mice and analyzed by Western blot using anti-p53 (top) and anti-actin (bottom) antibodies. (B) Mean±SE of relative mRNA level (normalized to Ctrl mice as 1) of p21, PUMA, Fas, PAX6 and STAT3 in neurospheres of Ctrl, FIP200hGFAP cKO, 2cKO, and p53hGFAP cKO mice are shown (n= 3 mice for each). (C, D) Mean±SE of the number (C) and size (D) of primary and secondary neurospheres from Ctrl, FIP200hGFAP cKO, 2cKO, and p53hGFAP cKO mice at P28 are shown (n=3 mice for each). (E-H) Neurospheres were frozen sectioned and analyzed by immunofluorescence for Nestin, Ki67, TUNEL, PAX6, phosphorylated STAT3, and DAPI, as indicated. Mean±SE of the percentage of Ki67+ (E), BrdU+ (F), and TUNEL+ (G) cells in neurospheres from Ctrl, FIP200hGFAP cKO, 2cKO, and p53hGFAP cKO mice are shown (n= 3 mice for each, counting of >500 cells for each mouse). Representative images are shown in H. *: p<0.01. Full-length blots are presented in the Supplementary Figure 11.