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. 2015 Oct;185(10):2843–2860. doi: 10.1016/j.ajpath.2015.06.014

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© 2015 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

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Polycystin (PC)-2 deficiency significantly up-regulates the Akt/MAPK signaling pathway. A: Duplicated protein lysates from the 9-month-old kidneys were immunoblotted with antibodies to phospho-Akt (pAkt) and total Akt (tAkt); phospho–c-serine/threonine-protein kinase (pc-Raf) and total c-Raf (tc-Raf); phospho– marker extraction kernel (pMEK)-1/2 and total MEK1/2 (tMEK1/2); and phospho-Erk1/2 (pErk1/2) and total Erk1/2; cleaved caspase (Casp)-3 and Casp3; β-actin (a protein-loading control). B: A normalized quantitative analysis was performed using the densitometry values from the Western blots for cleaved-casp3/casp3. Other normalized quantitative analyses of the densitometry values of pAkt/tAkt (C), pc-Raf/tc-Raf (D), pMEK1/2/tMEK1/2 (E), and pErk1/2/tErk1/2 (F) were also performed. Compared to the age-matched wild-type (WT) kidneys, the statistical analysis indicates significant up-regulation of Akt and its downstream factors in the Pkd2^−/−;PKD2^tg kidneys, but not in Pkd2^−/−;PKD2^tg/tg kidneys. Data expressed as means ± SD (B–F). ^∗∗P < 0.01, ^∗∗∗P < 0.001.