ArticleThe Journal of biological chemistry2011
The Krüppel-like factor 15 as a molecular link between myogenic factors and a chromosome 4q transcriptional enhancer implicated in facioscapulohumeral dystrophy.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 21 citations in OpenAlex.
- Transgenic mouse models for investigating human DUX4 expression during development and its roles in FSHD pathophysiology.Disease models & mechanisms · 2026Article
- The double homeodomain protein DUX4c is associated with regenerating muscle fibers and RNA-binding proteins.Skeletal muscle · 2023Article
- Article
- Overexpression of the double homeodomain protein DUX4c interferes with myofibrillogenesis and induces clustering of myonuclei.Skeletal muscle · 2018Article
- Polycomb repressive complex 1 provides a molecular explanation for repeat copy number dependency in FSHD muscular dystrophy.Human molecular genetics · 2017Article
- Sarcoma Cell Line Screen of Oncology Drugs and Investigational Agents Identifies Patterns Associated with Gene and microRNA Expression.Molecular cancer therapeutics · 2015Article
- Myogenic enhancers regulate expression of the facioscapulohumeral muscular dystrophy-associated DUX4 gene.Molecular and cellular biology · 2014Article
- Cancer-related genes in the transcription signature of facioscapulohumeral dystrophy myoblasts and myotubes.Journal of cellular and molecular medicine · 2014Article
- DUX4 promotes transcription of FRG2 by directly activating its promoter in facioscapulohumeral muscular dystrophy.Skeletal muscle · 2014Article
- Novel excitation-contraction coupling related genes reveal aspects of muscle weakness beyond atrophy-new hopes for treatment of musculoskeletal diseases.Frontiers in physiology · 2014Review
- Defective regulation of microRNA target genes in myoblasts from facioscapulohumeral dystrophy patients.The Journal of biological chemistry · 2013Article
- The glucocorticoid receptor and KLF15 regulate gene expression dynamics and integrate signals through feed-forward circuitry.Molecular and cellular biology · 2013Article
- DUX4 expression in FSHD muscle cells: how could such a rare protein cause a myopathy?Journal of cellular and molecular medicine · 2013Article
- A unique library of myogenic cells from facioscapulohumeral muscular dystrophy subjects and unaffected relatives: family, disease and cell function.European journal of human genetics : EJHG · 2012Article
- Asymmetric bidirectional transcription from the FSHD-causing D4Z4 array modulates DUX4 production.PloS one · 2012Article
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Facioscapulohumeral muscular dystrophy (FSHD), a dominant hereditary disease with a prevalence of 7 per 100,000 individuals, is associated with a partial deletion in the subtelomeric D4Z4 repeat array on chromosome 4q. The D4Z4 repeat contains a strong transcriptional enhancer that activates promoters of several FSHD-related genes. We report here that the enhancer within the D4Z4 repeat binds the Krüppel-like factor KLF15. KLF15 was found to be up-regulated during myogenic differentiation induced by serum starvation or by overexpression of the myogenic differentiation factor MYOD. When overexpressed, KLF15 activated the D4Z4 enhancer and led to overexpression of DUX4c (Double homeobox 4, centromeric) and FRG2 (FSHD region gene 2) genes, whereas its silencing caused inactivation of the D4Z4 enhancer. In immortalized human myoblasts, the D4Z4 enhancer was activated by the myogenic factor MYOD, an effect that was abolished upon KLF15 silencing or when the KLF15-binding sites within the D4Z4 enhancer were mutated, indicating that the myogenesis-related activation of the D4Z4 enhancer was mediated by KLF15. KLF15 and several myogenesis-related factors were found to be expressed at higher levels in myoblasts, myotubes, and muscle biopsies from FSHD patients than in healthy controls. We propose that KLF15 serves as a molecular link between myogenic factors and the activity of the D4Z4 enhancer, and it thus contributes to the overexpression of the DUX4c and FRG2 genes during normal myogenic differentiation and in FSHD.
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