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. 2010 Apr 5;30(11):2737–2749. doi: 10.1128/MCB.01566-09

FIG. 2.

FIG. 2.

CK2β positively controls forebrain NSC proliferation but did not interfere with NSC specification. (A) Analysis of RC2 (red) and GFAP (green) expressions by immunohistochemistry (IHC) in E18.5 wild-type and CK2βloxP/loxP, Nestin-cre telencephalons. Cell nuclei were stained with Hoechst dye 33342 (blue). (B) There was a significant reduction (***, P = 2.7 × 10−12 [3 embryos per genotype and 3 nonadjacent sections per ventricular zone {VZ}]) of BrdU+ S-phase NSCs in CK2βloxP/loxP, Nestin-cre VZs (outlined with a dotted line) of lateral ventricles compared to the number in wild-type controls, as well as a near absence of PH3-positive mitotic cells. (C) Caspase-3-dependent apoptosis analysis in E18.5 forebrains. Western blot analysis of cleaved PARP in E18.5 forebrain extracts. The control represents the staurosporine-treated (1 μM, 3 h) NIH 3T3 positive extract; cleaved PARP (arrow) serves as a marker of cells undergoing caspase-3-dependent apoptosis. Scale bars, 100 μm (A) and 50 μm (B).