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. Author manuscript; available in PMC: 2013 Jul 1.
Published in final edited form as: J Mol Neurosci. 2012 Jan 3;47(3):631–638. doi: 10.1007/s12031-011-9699-8

Figure 1.

Figure 1

(A). Left lanes: Spna2 immunoblots performed on spinal cord lysates from WT animals treated with vehicle or 1,2-DAB. The expression of the 150 kDa SBDP (Spna2 breakdown product) was increased in animals treated with 1,2-DAB. In contrast, the expression of the caspase specific 120 kDa SBDP seems to be decreased in animals treated with 1,2-DAB. Right lanes: Immunoblots for Spna2 mutant mice. Note the absence of the 150-kDa SBDP. A baseline expression of the 120 kDa SBDP in the vehicle-treated mice possibly occurs through a secondary Spna2 site for caspase-mediated proteolysis (Meary et. al., 2007). Gl-IIβ: loading control. (B) Densitometric evaluation of the immunosignal intensity of bands revealed a significant increase in the abundance (mean gray value ± SD) of the 150-kDa SBDP relative to that of the full-length 285-kDa Spna2 (** = p<0.005). (C) Densitometric findings revealed a significant reduction in the abundance (mean gray value ± SD) of the 120-kDa SBDP relative to that of the full-length Spna2 in both genotypes after treatment with 1,2-DAB (* = p<0.05).