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. Author manuscript; available in PMC: 2011 Feb 1.
Published in final edited form as: Glia. 2010 Feb;58(3):300–314. doi: 10.1002/glia.20924

Fig. 4.

Fig. 4

The huS100B transgene promotes amyloidogenic APP processing in Tg2576 mice. Data were obtained from Tg2576 [n = 14 (7 males and 7 females)] and Tg2576-huS100B mice [n = 16 (8 males and 8 females) at 15 months of age]. (A) Western blots using an N-terminal APP antibody (mAb 10D1, full-length holo-APP and soluble APP species are shown), a C-terminal β-site APP cleaving enzyme 1 antibody (pAb, BACE1), and an-N-terminal Aβ antibody [mAb 82E1, APP-C-terminal fragments generated by amyloidogenic APP cleavage (phospho-C99: P-β-CTF and C99: β-CTF) are shown]. Actin is shown as a loading control for each blot. (B) Densitometry analyses for the ratio of P-C99 or C99 to actin are shown. (C) Densitometry analysis for the ratio of BACE1 to actin is shown. (D) β-secretase activity analysis is shown. (E) The Tris-buffered saline (TBS)-soluble fraction from two-step extracted brain homogenates was also assayed by ELISA for soluble-APPβ. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Tg2576 mice.