HTRA1 Mutations Identified in Symptomatic Carriers Have the Property of Interfering the Trimer-Dependent Activation Cascade
- 1Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan
- 2Department of Medical Technology, Graduate School of Health Sciences, Niigata University, Niigata, Japan
- 3Division of Legal Medicine, Niigata University, Niigata, Japan
- 4Department of System Pathology for Neurological Disorders, Brain Research Institute, Niigata University, Niigata, Japan
A Corrigendum on
HTRA1 Mutations Identified in Symptomatic Carriers Have the Property of Interfering the Trimer-Dependent Activation Cascade
by Uemura, M., Nozaki, H., Koyama, A., Sakai, N., Ando, S., Kanazawa, M., Kato, T., and Onodera, O. (2019). Front. Neurol. 10:693. doi: 10.3389/fneur.2019.00693
In the original article, there were mistakes in Figures 1 and 3 as published. The multiplier of the unit for protease activity was incorrect. The correct value is 10 to the third power. The corrected Figures 1 and 3 appear below.
Figure 1. Protease activity of missense HTRA1s identified in symptomatic carriers. (A) SDS-PAGE of WT and missense mutant HTRA1 proteins used in the protease assay. Black arrows indicate the full-length band of HTRA1 tagged with myc-His6. (B) Protease activities of missense HTRA1s identified in symptomatic carriers and CARASIL patients. Activities were calculated from the slope of the linear portion of the normalized fluorescence vs. time (30, 60, 90 min) plots. Mean values from 3 independent experiments are shown. Red and blue bars indicate protease activities of WT and S328A, the positive and negative controls, respectively. Green bars indicate protease activities of missense HTRA1s identified in symptomatic carriers. Purple bars indicate protease activities of missense HTRA1s identified only in CARASIL patients. I-bars indicate standard errors (SE). Statistical comparisons of protease activities between WT and each missense HTRA1 protein were performed with one-way analysis of variance followed by the Dunnett's post hoc test. ***P < 0.0001 for protease activities of each HTRA1 relative to WT. ##P < 0.0001 for protease activities of HTRA1 relative to WT.
Figure 3. Dominant-negative effects of missense HTRA1s identified in symptomatic carriers. Protease activities of mixtures of each missense HTRA1 with WT calculated from the slope of the linear portion of normalized fluorescence vs. time (30, 60, and 90 min) plots. Orange, S328A/WT, a positive control for a dominant-negative effect. Blue and red bars indicate protease activities of A252T/WT and G283E/WT, respectively, negative and positive controls for dominant-negative effect, respectively. Green bars, missense HTRA1s identified in symptomatic carriers. Purple bars, missense HTRA1s found only in CARASIL patients. I-bars indicate standard errors (SE). Statistical comparisons of protease activities between each mutant HTRA1/WT and S328A/WT were performed with one-way analysis of variance followed by Dunnett's post hoc test. ***P < 0.0001; *P < 0.05 for increases in protease activities for each HTRA1/WT relative to S328A/WT. ##P < 0.0001; #p < 0.05 for differences for HTRA1/WT mixtures relative to S328A/WT.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Keywords: heritability, vascular dementia, mutations, HTRA1, carriers, CARASIL
Citation: Uemura M, Nozaki H, Koyama A, Sakai N, Ando S, Kanazawa M, Kato T and Onodera O (2021) Corrigendum: HTRA1 Mutations Identified in Symptomatic Carriers Have the Property of Interfering the Trimer-Dependent Activation Cascade. Front. Neurol. 12:756038. doi: 10.3389/fneur.2021.756038
Received: 09 August 2021; Accepted: 10 August 2021;
Published: 08 September 2021.
Approved by:
Frontiers Editorial Office, Frontiers Media SA, SwitzerlandCopyright © 2021 Uemura, Nozaki, Koyama, Sakai, Ando, Kanazawa, Kato and Onodera. 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.
*Correspondence: Osamu Onodera, onodera@bri.niigata-u.ac.jp