ArticleCirculation research2009
Transient expression of FRNK reveals stage-specific requirement for focal adhesion kinase activity in cardiac growth.
Article in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Reversing metabolic reprogramming by CPT1 inhibition with etomoxir promotes cardiomyocyte proliferation and heart regenerationActa pharmaceutica Sinica. B · 2025Article
- Focal Adhesion's Role in Cardiomyocytes Function: From Cardiomyogenesis to Mechanotransduction.Cells · 2024Review
- Polycomb Group Protein CBX7 Represses Cardiomyocyte Proliferation Through Modulation of the TARDBP/RBM38 Axis.Circulation · 2023Article
- Endothelial Loss of ETS1 Impairs Coronary Vascular Development and Leads to Ventricular Non-Compaction.Circulation research · 2022Article
- Carpaine Promotes Proliferation and Repair of H9c2 Cardiomyocytes after Oxidative Insults.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Molecular Regulation of the RhoGAP GRAF3 and Its Capacity to Limit Blood Pressure In Vivo.Cells · 2020Article
- Potential Common Pathogenic Pathways for the Left Ventricular Noncompaction Cardiomyopathy (LVNC).Pediatric cardiology · 2018Article
- Regulation of Focal Adhesion Kinase through a Direct Interaction with an Endogenous Inhibitor.Biochemistry · 2017Article
- TRIM9-dependent ubiquitination of DCC constrains kinase signaling, exocytosis, and axon branching.Molecular biology of the cell · 2017Article
- Focal Adhesion Kinase-mediated Phosphorylation of Beclin1 Protein Suppresses Cardiomyocyte Autophagy and Initiates Hypertrophic Growth.The Journal of biological chemistry · 2017Article
- iPSC-derived cardiomyocytes reveal abnormal TGF-β signalling in left ventricular non-compaction cardiomyopathy.Nature cell biology · 2016Article
- Genetics of Cardiac Developmental Disorders: Cardiomyocyte Proliferation and Growth and Relevance to Heart Failure.Annual review of pathology · 2016Review
- GRAF1 promotes ferlin-dependent myoblast fusion.Developmental biology · 2014Article
- Integrins and integrin-associated proteins in the cardiac myocyte.Circulation research · 2014Review
- From stem cells to cardiomyocytes: the role of forces in cardiac maturation, aging, and disease.Progress in molecular biology and translational science · 2014Review
- New approaches to prevent LEOPARD syndrome-associated cardiac hypertrophy by specifically targeting Shp2-dependent signaling.The Journal of biological chemistry · 2013Article
- Microdomain heterogeneity in 3D affects the mechanics of neonatal cardiac myocyte contraction.Biomechanics and modeling in mechanobiology · 2013Article
- The smooth muscle-selective RhoGAP GRAF3 is a critical regulator of vascular tone and hypertension.Nature communications · 2013Article
- Germline deletion of FAK-related non-kinase delays post-natal cardiomyocyte mitotic arrest.Journal of molecular and cellular cardiology · 2012Article
- Targeted focal adhesion kinase activation in cardiomyocytes protects the heart from ischemia/reperfusion injury.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Focal adhesion kinase (FAK) is strongly activated by integrins and growth factors and is essential for embryonic development. We previously showed that the C terminus of FAK is expressed as a separate protein termed FAK-related nonkinase (FRNK) in a smooth muscle cell-selective fashion and that FRNK functions to buffer FAK-dependent signals. We now show that FRNK is also transiently expressed in the neonatal myocardium, with peak levels occurring 5 to 7 days postnatal, just before cell cycle withdrawal. Using novel mouse models, we demonstrate that cardiac-selective expression of FRNK (leading to inhibition of FAK) starting at embryonic day 10.5 leads to a severe ventricular noncompaction defect associated with reduced cardiomyocyte proliferation. Remarkably, postnatal expression of nearly identical levels of FRNK is well tolerated and does not affect viability or anabolic cardiac growth. Nonetheless, FRNK expression in the adult heart does attenuate pathological cardiac hypertrophy following aortic banding, confirming and extending our previous data that this compensatory response is blunted in FAK null hearts. Our mechanistic studies in cultured neonatal cardiomyocytes reveal that FRNK expression induces p38/p27(kip)-dependent cell cycle withdrawal and attenuates extracellular signal-regulated kinase-dependent hypertrophic growth. These findings indicate that dynamic expression of FRNK in the neonatal heart may function to promote cardiomyocyte quiescence in an environment that is particularly rich in growth factors and growth promoting extracellular matrices.
Indexed as
Identifiers
What OpenQuestion holds
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.