ArticleMolecular and cellular biology2007
Conditional deletion of focal adhesion kinase leads to defects in ventricular septation and outflow tract alignment.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 64 citations in OpenAlex.
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- 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
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- Endocytic Protein Defects in the Neural Crest Cell Lineage and Its Pathway Are Associated with Congenital Heart Defects.International journal of molecular sciences · 2021Review
- Muscularization of the Mesenchymal Outlet Septum during Cardiac Development.Journal of cardiovascular development and disease · 2020Review
- De novo variants in exomes of congenital heart disease patients identify risk genes and pathways.Genome medicine · 2020Article
- Mature miR-99a Upregulation in the Amniotic Fluid Samples from Female Fetus Down Syndrome Pregnancies: A Pilot Study.Medicina (Kaunas, Lithuania) · 2019Article
- 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
- SRChing for the substrates of Src.Oncogene · 2014Review
- Focal adhesion signaling in heart failure.Pflugers Archiv : European journal of physiology · 2014Review
- Proteomic profiling of endothelial invasion revealed receptor for activated C kinase 1 (RACK1) complexed with vimentin to regulate focal adhesion kinase (FAK).The Journal of biological chemistry · 2013Article
- Human embryonic stem cell-derived cardiomyocytes migrate in response to gradients of fibronectin and Wnt5a.Stem cells and development · 2013Article
- ErbB/integrin signaling interactions in regulation of myocardial cell-cell and cell-matrix interactions.Biochimica et biophysica acta · 2013Review
- Article
- Partitioning the heart: mechanisms of cardiac septation and valve development.Development (Cambridge, England) · 2012Review
- Germline deletion of FAK-related non-kinase delays post-natal cardiomyocyte mitotic arrest.Journal of molecular and cellular cardiology · 2012Article
- Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy.Journal of molecular and cellular cardiology · 2012Article
- Quantification of myocyte chemotaxis: a role for FAK in regulating directional motility.Methods in molecular biology (Clifton, N.J.) · 2012Article
- WT1-interacting protein (Wtip) regulates podocyte phenotype by cell-cell and cell-matrix contact reorganization.American journal of physiology. Renal physiology · 2012Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
To examine a role for focal adhesion kinase (FAK) in cardiac morphogenesis, we generated a line of mice with a conditional deletion of FAK in nkx2-5-expressing cells (herein termed FAKnk mice). FAKnk mice died shortly after birth, likely resulting from a profound subaortic ventricular septal defect and associated malalignment of the outflow tract. Additional less penetrant phenotypes included persistent truncus arteriosus and thickened valve leaflets. Thus, conditional inactivation of FAK in nkx2-5-expressing cells leads to the most common congenital heart defect that is also a subset of abnormalities associated with tetralogy of Fallot and the DiGeorge syndrome. No significant differences in proliferation or apoptosis between control and FAKnk hearts were observed. However, decreased myocardialization was observed for the conal ridges of the proximal outflow tract in FAKnk hearts. Interestingly, chemotaxis was significantly attenuated in isolated FAK-null cardiomyocytes in comparison to genetic controls, and these effects were concomitant with reduced tyrosine phosphorylation of Crk-associated substrate (CAS). Thus, it is possible that ventricular septation and appropriate outflow tract alignment is dependent, at least in part, upon FAK-dependent CAS activation and subsequent induction of polarized myocyte movement into the conal ridges. Future studies will be necessary to determine the precise contributions of the additional nkx2-5-derived lineages to the phenotypes observed.
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Registered trials
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