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. Author manuscript; available in PMC: 2013 Nov 2.
Published in final edited form as: Oncogene. 2012 Jun 18;32(18):2304–2314. doi: 10.1038/onc.2012.248

Figure 2. Bax deficient CGNPs have normal response to Shh but altered response to pro-apoptotic stimulus.

Figure 2

A) A representative Western blot demonstrates temporal expression patterns of indicated proteins in lysates of whole cerebella harvested from Bax+/+ and Bax−/− littermates at the ages indicated, with β-Actin used as a loading control. While Cyclin D2 elevation waned more slowly in Bax−/− mice, Shh abundance remained constant over time and did not vary with genotype. Differential expression of Cyclin D2 was noted in at least 3 paired Bax+/+ and Bax−/− littermates at each time point from P11-P17. B) Comparison of proliferation of CGNPs isolated from Bax+/+ and Bax−/− littermates and cultured in the presence or absence of exogenous Shh, measured by Western blot for Cyclin D2, demonstrated that proliferative response to Shh was not affected by Bax deletion. 3 replicate wells for each condition demonstrated equivalent findings. C) Representative Western blot comparing apoptosis induced by dexamethasone in Bax+/+ and Bax−/− littermates, detected by cC3 in whole cerebellar lysates 24 hours after IP injection of dexamethasone or saline. D) Examination of Bcl-2 family proteins over CGNP development, in Bax+/+ and Bax−/− mice. A SmoA1-induced medulloblastoma is included for comparison.