Generation of two human iPSC lines with Exon 3 mutations in BCL2-Associated Athanogene 3 (BAG3) from dilated cardiomyopathy patients

Dilated cardiomyopathies (DCM) are one of the main causes of heart failure as one ages. BAG3 is a chaperone protein that is heavily implicated in the development of DCM and speed of progression toward heart failure. Here we generate two human iPSC lines from individuals with mutations in exon 3 of B...

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Autores principales: Zushin, Peter-James H., Zhou, Yang, Li, Audrey, Ashley, Euan A., Wheeler, Matthew T., Wu, Joseph C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2023
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10042224/
https://www.ncbi.nlm.nih.gov/pubmed/36642055
http://dx.doi.org/10.1016/j.scr.2023.103019
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author Zushin, Peter-James H.
Zhou, Yang
Li, Audrey
Ashley, Euan A.
Wheeler, Matthew T.
Wu, Joseph C.
author_facet Zushin, Peter-James H.
Zhou, Yang
Li, Audrey
Ashley, Euan A.
Wheeler, Matthew T.
Wu, Joseph C.
author_sort Zushin, Peter-James H.
collection PubMed
description Dilated cardiomyopathies (DCM) are one of the main causes of heart failure as one ages. BAG3 is a chaperone protein that is heavily implicated in the development of DCM and speed of progression toward heart failure. Here we generate two human iPSC lines from individuals with mutations in exon 3 of BAG3 and provide validation of their pluripotency and ability to differentiate toward the three primary germ layers. These two cell lines can help our understanding of BAG3 and its role in DCM by providing a good model for BAG3 inactivation and insufficiency.
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spelling pubmed-100422242023-03-27 Generation of two human iPSC lines with Exon 3 mutations in BCL2-Associated Athanogene 3 (BAG3) from dilated cardiomyopathy patients Zushin, Peter-James H. Zhou, Yang Li, Audrey Ashley, Euan A. Wheeler, Matthew T. Wu, Joseph C. Stem Cell Res Article Dilated cardiomyopathies (DCM) are one of the main causes of heart failure as one ages. BAG3 is a chaperone protein that is heavily implicated in the development of DCM and speed of progression toward heart failure. Here we generate two human iPSC lines from individuals with mutations in exon 3 of BAG3 and provide validation of their pluripotency and ability to differentiate toward the three primary germ layers. These two cell lines can help our understanding of BAG3 and its role in DCM by providing a good model for BAG3 inactivation and insufficiency. 2023-03 2023-01-05 /pmc/articles/PMC10042224/ /pubmed/36642055 http://dx.doi.org/10.1016/j.scr.2023.103019 Text en https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ).
spellingShingle Article
Zushin, Peter-James H.
Zhou, Yang
Li, Audrey
Ashley, Euan A.
Wheeler, Matthew T.
Wu, Joseph C.
Generation of two human iPSC lines with Exon 3 mutations in BCL2-Associated Athanogene 3 (BAG3) from dilated cardiomyopathy patients
title Generation of two human iPSC lines with Exon 3 mutations in BCL2-Associated Athanogene 3 (BAG3) from dilated cardiomyopathy patients
title_full Generation of two human iPSC lines with Exon 3 mutations in BCL2-Associated Athanogene 3 (BAG3) from dilated cardiomyopathy patients
title_fullStr Generation of two human iPSC lines with Exon 3 mutations in BCL2-Associated Athanogene 3 (BAG3) from dilated cardiomyopathy patients
title_full_unstemmed Generation of two human iPSC lines with Exon 3 mutations in BCL2-Associated Athanogene 3 (BAG3) from dilated cardiomyopathy patients
title_short Generation of two human iPSC lines with Exon 3 mutations in BCL2-Associated Athanogene 3 (BAG3) from dilated cardiomyopathy patients
title_sort generation of two human ipsc lines with exon 3 mutations in bcl2-associated athanogene 3 (bag3) from dilated cardiomyopathy patients
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10042224/
https://www.ncbi.nlm.nih.gov/pubmed/36642055
http://dx.doi.org/10.1016/j.scr.2023.103019
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