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. 2019 Aug 27;10:2000. doi: 10.3389/fimmu.2019.02000

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At least a portion of this work is authored by Jeffrey I. Cohen on behalf of the U.S. Government and, as regards Dr. Cohen and the U.S. Government, is not subject to copyright protection in the United States. Foreign and other copyrights may apply.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ITK mutation in the patient. (A) ITK protein is present in the patient's peripheral blood mononuclear cells at a similar level to control. Actin is a protein loading control. (B) The root mean square fluctuation (RMSF) for wild-type ITK (WT) and the mutant ITK in the patient (D540N) is shown with the 80% confidence interval highlighted. (C) Average structure from the simulations, displaying the increased flexibility of the ITK kinase domain, which causes the alpha helical turns in residues 504–506 and residues 510 to 513 to be missing from the mutant compared to the WT ITK, indicated by the green arrow. The residues are colored according to their RMSF values, with blue representing low-, green representing the mid- and red representing the high-RMSF values.