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The phenotypes of  calbindin-D9k - ( CaBP-9k -) knockout (KO),  calbindin - D28k - ( CaBP-28k -) KO, and  CaBP-9k/28k -KO mice are similar to those of wild-type (WT) mice due to the compensatory action of other calcium transport proteins. In this study, we investigated the expression of cellular prion protein (PrP C ) in the brains of  CaBP-9k -,  CaBP-28k -, and  CaBP-9k/28k -KO mice. PrP C  expression was significantly upregulated in the brain of all three strains. Levels of phospho-Akt (Ser473) and phospho-Bad (Ser136) were significantly elevated, but those of phospho-ERK and phospho-Bad (Ser155 and 112) were significantly reduced in the brains of  CaBP-9k -,  CaBP-28k -, and  CaBP-9k/28k -KO mice. The expressions of the Bcl-2, p53, Bax, Cu/Zn-SOD, and Mn-SOD proteins were decreased in the brains of all KO mice. Expression of the endoplasmic reticulum marker protein BiP/GRP78 was decreased, and that of the CHOP protein was increased in the brains of those KO mice. To identify the roles of  CaBP-28k , we transfected PC12 cells with siRNA for  CaBP-28k  and found increased expression of the PrP C  protein compared to the levels in control cells. These results suggest that  CaBP-28k  expression may regulate PrP C  protein expression and these mice may be vulnerable to the influence of prion disease.

Calbindin-D28kin the Brain Influences the Expression of Cellular Prion Protein