ArticleThe EMBO journal2006
The Kruppel-like transcription factor KLF13 is a novel regulator of heart development.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Advancing our understanding of genetic risk factors and potential personalized strategies for pelvic organ prolapse.Nature communications · 2022Pooled it
- Review
- Article
- Review
- A new KLF13 loss-of-function mutation responsible for sporadic dilated cardiomyopathy.Molecular biology reports · 2025Article
- Mitotic block and epigenetic repression underlie neurodevelopmental defects and neurobehavioral deficits in congenital heart disease.Nature communications · 2025Article
- KLF13 restrains Dll4-muscular Notch2 axis to improve the muscle atrophy.Journal of cachexia, sarcopenia and muscle · 2024Article
- Krüppel-like factors family in health and disease.MedComm · 2024Review
- Bioinformatic Evaluation ofGenes · 2024Article
- Is the Cis-Element CACCC-Box a Master Regulatory Element during Cardiovascular Disease? A Bioinformatics Approach from the Perspective of the Krüppel-like Family of Transcription Factors.Life (Basel, Switzerland) · 2024Article
- A Functional Single-Nucleotide Polymorphism Upstream of the Collagen Type III Gene Is Associated with Catastrophic Fracture Risk in Thoroughbred Horses.Animals : an open access journal from MDPI · 2023Article
- Review
- Long non-coding RNA DANCR alleviates acute myocardial infarction damage via regulating microRNA-509-5p/KLF transcription factor 13 pathway.The Kaohsiung journal of medical sciences · 2023Article
- Specificity Proteins (SP) and Krüppel-like Factors (KLF) in Liver Physiology and Pathology.International journal of molecular sciences · 2023Review
- The Profiles and Functions of RNA Editing Sites Associated with High-Altitude Adaptation in Goats.International journal of molecular sciences · 2023Article
- The Involvement of Krüppel-like Factors in Cardiovascular Diseases.Life (Basel, Switzerland) · 2023Review
- KLF13 overexpression protects sepsis-induced myocardial injury and LPS-induced inflammation and apoptosis.International journal of experimental pathology · 2023Article
- Kruppel-like Factors in Skeletal Physiology and Pathologies.International journal of molecular sciences · 2022Review
- KLF13 Loss-of-Function Mutations Underlying Familial Dilated Cardiomyopathy.Journal of the American Heart Association · 2022Article
- Kruppel-like factor 13 inhibits cell proliferation of gastric cancer by inducing autophagic degradation of β-catenin.Discover oncology · 2022Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In humans, congenital heart defects occur in 1-2% of live birth, but the molecular mechanisms and causative genes remain unidentified in the majority of cases. We have uncovered a novel transcription pathway important for heart morphogenesis. We report that KLF13, a member of the Krüppel-like family of zinc-finger proteins, is expressed predominantly in the heart, binds evolutionarily conserved regulatory elements on cardiac promoters and activates cardiac transcription. KLF13 is conserved across species and knockdown of KLF13 in Xenopus embryos leads to atrial septal defects and hypotrabeculation similar to those observed in humans or mice with hypomorphic GATA-4 alleles. Physical and functional interaction with GATA-4, a dosage-sensitive cardiac regulator, provides a mechanistic explanation for KLF13 action in the heart. The data demonstrate that KLF13 is an important component of the transcription network required for heart development and suggest that KLF13 is a GATA-4 modifier; by analogy to other GATA-4 collaborators, mutations in KLF13 may be causative for congenital human heart disease.
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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.