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Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development

Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5544300

Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development

About this item

Full title

Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development

Publisher

United States: National Academy of Sciences

Journal title

Proceedings of the National Academy of Sciences - PNAS, 2017-07, Vol.114 (30), p.8029-8034

Language

English

Formats

Publication information

Publisher

United States: National Academy of Sciences

More information

Scope and Contents

Contents

GAS2L3 is a recently identified cytoskeleton-associated protein that interacts with actin filaments and tubulin. The in vivo function of GAS2L3 in mammals remains unknown. Here, we show that mice deficient in GAS2L3 die shortly after birth because of heart failure. Mammalian cardiomyocytes lose the ability to proliferate shortly after birth, and fu...

Alternative Titles

Full title

Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5544300

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5544300

Other Identifiers

ISSN

0027-8424

E-ISSN

1091-6490

DOI

10.1073/pnas.1703406114

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