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. 2013 Jan 22;41(5):3240–3256. doi: 10.1093/nar/gks1227

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© The Author(s) 2013. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — The level of full-length CREB is decreased in AD brain and is correlated to activation of calpain I in human brain. (A) Western blots of CREB, calpain I and CaN A. Frontal cortical homogenates from seven AD and seven control cases were subjected to western blots developed with antibodies against CREB, calpain I, CaN A or GAPDH. (B) The level of full-length CREB was decreased and truncation of CREB was increased in AD brain significantly. Blots as shown in (A) developed with anti-CREB (upper panel) were quantitated by densitometry, and the levels of CREB was normalized with GAPDH and presented as mean ± SD; *P < 0.05; **P < 0.01. (C) Truncation and activation of calpain I were significantly increased in AD brain. Arrow indicates full length of calpain I and vertical line indicates truncated and active form of calpain I. Blots as shown in (A) developed with anti-calpain I were quantitated by densitometry, the truncation and activation of calpain I were presented by the ratio of the truncated (76–78 kDa) over the total calpain I. (D) CREB level was correlated with the activation of calpain I in human brain. The relative activation of calpain I [truncated/(full length + truncated)] (x-axis) is plotted against the relative CREB level (y-axis).