ArticlePLoS genetics2013
ENU-induced mutation in the DNA-binding domain of KLF3 reveals important roles for KLF3 in cardiovascular development and function in mice.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Bone mesenchymal stem cells (BMSCs)-derived exosomal microRNA-21-5p regulates Kruppel-like factor 3 (KLF3) to promote osteoblast proliferationBioengineered · 2022Article
- Lack of food intake during shift work alters the heart transcriptome and leads to cardiac tissue fibrosis and inflammation in rats.BMC biology · 2022Article
- Chromatin Accessibility of Human Mitral Valves and Functional Assessment of MVP Risk Loci.Circulation research · 2021Article
- KLF3 promotes the 8-cell-like transcriptional state in pluripotent stem cells.Cell proliferation · 2020Article
- Molecular Signatures and Networks of Cardiomyocyte Differentiation in Humans and Mice.Molecular therapy. Nucleic acids · 2020Article
- Salvia miltiorrhiza-Derived Sal-miR-58 Induces Autophagy and Attenuates Inflammation in Vascular Smooth Muscle Cells.Molecular therapy. Nucleic acids · 2020Article
- Ophiopogonin D promotes bone regeneration by stimulating CD31Cell proliferation · 2020Article
- Krüppel-like factor 3 inhibition by mutated lncRNAThe Journal of experimental medicine · 2019Article
- Corrupted DNA-binding specificity and ectopic transcription underpin dominant neomorphic mutations in KLF/SP transcription factors.BMC genomics · 2019Article
- Article
- Krüppel-like factors: Crippling and un-crippling metabolic pathways.JACC. Basic to translational science · 2018Article
- Heart morphogenesis gene regulatory networks revealed by temporal expression analysis.Development (Cambridge, England) · 2017Article
- RNA sequencing analysis reveals protective role of kruppel-like factor 3 in colorectal cancer.Oncotarget · 2017Article
- Krüppel-like factors in mammalian stem cells and development.Development (Cambridge, England) · 2017Review
- Promiscuous DNA-binding of a mutant zinc finger protein corrupts the transcriptome and diminishes cell viability.Nucleic acids research · 2017Article
- Krüppel-like Factor 3 (KLF3/BKLF) Is Required for Widespread Repression of the Inflammatory Modulator Galectin-3 (Lgals3).The Journal of biological chemistry · 2016Article
- Epigenetic silencing of Kruppel like factor-3 increases expression of pro-metastatic miR-182.Cancer letters · 2015Article
- Kruppel-like factors in muscle health and disease.Trends in cardiovascular medicine · 2015Review
- Phosphorylation of Krüppel-like factor 3 (KLF3/BKLF) and C-terminal binding protein 2 (CtBP2) by homeodomain-interacting protein kinase 2 (HIPK2) modulates KLF3 DNA binding and activity.The Journal of biological chemistry · 2015Article
- Cardiovascular Patterning as Determined by Hemodynamic Forces and Blood Vessel Genetics.PloS one · 2015Article
Corrections and comments
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Authors and funding
25 authors at 8 institutions in 3 countries.
Funding
Abstract
KLF3 is a Krüppel family zinc finger transcription factor with widespread tissue expression and no previously known role in heart development. In a screen for dominant mutations affecting cardiovascular function in N-ethyl-N-nitrosourea (ENU) mutagenized mice, we identified a missense mutation in the Klf3 gene that caused aortic valvular stenosis and partially penetrant perinatal lethality in heterozygotes. All homozygotes died as embryos. In the first of three zinc fingers, a point mutation changed a highly conserved histidine at amino acid 275 to arginine (Klf3(H275R) ). This change impaired binding of the mutant protein to KLF3's canonical DNA binding sequence. Heterozygous Klf3(H275R) mutants that died as neonates had marked biventricular cardiac hypertrophy with diminished cardiac chambers. Adult survivors exhibited hypotension, cardiac hypertrophy with enlarged cardiac chambers, and aortic valvular stenosis. A dominant negative effect on protein function was inferred by the similarity in phenotype between heterozygous Klf3(H275R) mutants and homozygous Klf3 null mice. However, the existence of divergent traits suggested the involvement of additional interactions. We conclude that KLF3 plays diverse and important roles in cardiovascular development and function in mice, and that amino acid 275 is critical for normal KLF3 protein function. Future exploration of the KLF3 pathway provides a new avenue for investigating causative factors contributing to cardiovascular disorders in humans.
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