ArticleThe Journal of clinical investigation2009
Focal adhesion kinase is required for neural crest cell morphogenesis during mouse cardiovascular development.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Functional genomics iniScience · 2026Article
- Focal adhesion proteins confer smooth muscle anoikis resistance and protection against aortic aneurysm and dissection.JCI insight · 2026Article
- Integrative Functional Genomics Identifies ARHGAP10 in the 4q31.2 Locus as a Novel Congenital Heart Disease and Ciliopathy Gene.bioRxiv : the preprint server for biology · 2025Article
- Crk and Crkl have shared functions in neural crest cells for cardiac outflow tract septation and vascular smooth muscle differentiation.Human molecular genetics · 2022Article
- IL-7-induced phosphorylation of the adaptor Crk-like and other targets.Cellular signalling · 2018Article
- Co-culture with neonatal cardiomyocytes enhances the proliferation of iPSC-derived cardiomyocytes via FAK/JNK signaling.BMC developmental biology · 2016Article
- Neural crest cell-autonomous roles of fibronectin in cardiovascular development.Development (Cambridge, England) · 2016Article
- Neural crest-derived SEMA3C activates endothelial NRP1 for cardiac outflow tract septation.The Journal of clinical investigation · 2015Article
- α5 and αv integrins cooperate to regulate vascular smooth muscle and neural crest functions in vivo.Development (Cambridge, England) · 2015Article
- The Q510E mutation in Shp2 perturbs heart valve development by increasing cell migration.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Article
- Mesodermal expression of integrin α5β1 regulates neural crest development and cardiovascular morphogenesis.Developmental biology · 2014Article
- SRChing for the substrates of Src.Oncogene · 2014Review
- Novel TBX1 loss-of-function mutation causes isolated conotruncal heart defects in Chinese patients without 22q11.2 deletion.BMC medical genetics · 2014Article
- Mechanosensing and Regulation of Cardiac Function.Journal of clinical & experimental cardiology · 2014Article
- Identification of novel candidate gene loci and increased sex chromosome aneuploidy among infants with conotruncal heart defects.American journal of medical genetics. Part A · 2014Article
- Requirement for integrin-linked kinase in neural crest migration and differentiation and outflow tract morphogenesis.BMC biology · 2013Article
- Deletion of integrin-linked kinase from neural crest cells in mice results in aortic aneurysms and embryonic lethality.Disease models & mechanisms · 2013Article
- Neural crest cells are required for correct positioning of the developing outflow cushions and pattern the arterial valve leaflets.Cardiovascular research · 2013Article
- Cardiac outflow tract anomalies.Wiley interdisciplinary reviews. Developmental biology · 2013Review
- Murine craniofacial development requires Hdac3-mediated repression of Msx gene expression.Developmental biology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Neural crest cells (NCCs) participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Focal adhesion kinase (FAK) mediates signal transduction by integrin and growth factor receptors, each of which is important for normal cardiovascular development. To investigate the role of FAK in NCC morphogenesis, we deleted it in murine NCCs using Wnt1cre, yielding craniofacial and cardiovascular malformations resembling those observed in individuals with DiGeorge syndrome. In these mice, we observed normal cardiac NCC migration but reduced differentiation into smooth muscle within the aortic arch arteries and impaired cardiac outflow tract rotation, which resulted in a dextroposed aortic root. Moreover, within the conotruncal cushions, Fak-deficient NCCs formed a less organized mesenchyme, with reduced expression of perlecan and semaphorin 3C, and exhibited disorganized F-actin stress fibers within the aorticopulmonary septum. Additionally, absence of Fak resulted in reduced in vivo phosphorylation of Crkl and Erk1/2, components of a signaling pathway essential for NCC development. Consistent with this, both TGF-beta and FGF induced FAK and Crkl phosphorylation in control but not Fak-deficient NCCs in vitro. Our results indicate that FAK plays an essential role in cardiac outflow tract development by promoting the activation of molecules such as Crkl and Erk1/2.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.