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CORRECTION article

Front. Cardiovasc. Med., 16 August 2024
Sec. Cardiovascular Genetics and Systems Medicine

Corrigendum: a novel αB-crystallin R123W variant drives hypertrophic cardiomyopathy by promoting maladaptive calcium-dependent signal transduction

\r\nChun ChouChun Chou1Gregory L. MartinGregory L. Martin2Gayani PereraGayani Perera2Junya AwataJunya Awata2Amy LarsonAmy Larson2Robert Blanton,Robert Blanton1,2Michael T. Chin,
\r\nMichael T. Chin1,2*
  • 1Department of Medicine, Tufts University School of Medicine, Boston, MA, United States
  • 2Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA, United States

A corrigendum on

A novel αB-crystallin R123W variant drives hypertrophic cardiomyopathy by promoting maladaptive calcium-dependent signal transduction

By Chou C, Martin GL, Perera G, Awata J, Larson A, Blanton R, Chin MT (2023). Front. Cardiovasc. Med. 10:1223244. doi: 10.3389/fcvm.2023.1223244

Text Correction

In the published article, there was an error. The methods section inadvertently omitted the sentence “The CryabR123W and Mybc3Trunc mice were generated at the Maine Health Institute for Research Mouse Genome Modification Core Facility https://mhir.org/?page_id = 233.”

A correction has been made to Methods, Mice, Paragraph Number 1. This sentence previously stated:

“Myh6/NFAT-luc [FVB-Tg(Myh6/NFAT-luc)1 Jmol/J] reporter mice were purchased from Jackson Laboratories. The CryabR123W allele was generated via homology directed repair using the CRISPR/Cas9 system. Briefly, a guide RNA (GATCCACATCGGCT GGGATCCGG), single-stranded oligodeoxynucleotides (ssODN) donor template containing the CGG to TGG mutation, and mRNA encoding Cas9 were co-injected into the cytoplasm/pronucleus of single cell embryos.”

The corrected section appears below:

“Myh6/NFAT-luc [FVB-Tg(Myh6/NFAT-luc)1 Jmol/J] reporter mice were purchased from Jackson Laboratories. The CryabR123W and Mybc3Trunc mice were generated at the Maine Health Institute for Research Mouse Genome Modification Core Facility https://mhir.org/?page_id = 233. The CryabR123W allele was generated via homology directed repair using the CRISPR/Cas9 system. Briefly, a guide RNA (GATCCACATCGGCT GGGATCCGG), single-stranded oligodeoxynucleotides (ssODN) donor template containing the CGG to TGG mutation, and mRNA encoding Cas9 were co-injected into the cytoplasm/pronucleus of single cell embryos.”

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.

Publisher's note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Keywords: hypertrophic cardiomyopathy, cardiac hypertrophy, cryab, calcineurin, NFAT, transverse aortic constriction, cardiac fibrosis

Citation: Chou C, Martin GL, Perera G, Awata J, Larson A, Blanton R and Chin MT (2024) Corrigendum: a novel αB-crystallin R123W variant drives hypertrophic cardiomyopathy by promoting maladaptive calcium-dependent signal transduction. Front. Cardiovasc. Med. 11:1455263. doi: 10.3389/fcvm.2024.1455263

Received: 26 June 2024; Accepted: 27 June 2024;
Published: 16 August 2024.

Approved by: Frontiers Editorial office, Frontiers Media SA, Switzerland

Copyright: © 2024 Chou, Martin, Perera, Awata, Larson, Blanton and Chin. 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: Michael T. Chin, bWNoaW4zQHR1ZnRzbWVkaWNhbGNlbnRlci5vcmc=

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.