Ann Intern Med. 2008;149(1): doi: / Figure Legend:

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From: Cardiac JAK2 Mutation V617F in a Patient with Cardiomyopathy and Myeloproliferative Disease Ann Intern Med. 2008;149(1):69-71. doi:10.7326/0003-4819-149-1-200807010-00027 Figure Legend: Detection of phosphoSTAT3 (pSTAT3) in the patient's JAK2mutV617F-positive right and left cardiac ventricle (RVJAK2-V617F, LVJAK2-V617F) by Western blot (a) and immunohistochemistry (b and c, nuclear staining, left ventricle). Absence of pSTAT3 in JAK2 wild-type control hearts (n = 14) (a, RVJAK2-wt, LVJAK2-wt; c, LVJAK2-wt). GAPDH is the protein loading control. Murine HL-1 cardiomyocytes transfected with JAK2mutV617F showed increased nuclear pSTAT3 expression (d, HL-1 JAK2mutV617F red fluorescence), whereas HL-1 cardiomyocytes transfected with JAK2 wild type remained largely pSTAT3 negative (e, HL-1 JAK2wt red fluorescence). Transfection with green fluorescence protein served as control for transfection efficiency (about 30%) (Alexa 488 and Cy3, × 400.) Date of download: 11/13/2017 Copyright © American College of Physicians. All rights reserved.

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