ArticleMolecular and cellular neurosciences2012
The T3-induced gene KLF9 regulates oligodendrocyte differentiation and myelin regeneration.
Article in Molecular and cellular neurosciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
- Epigenome-Wide Association Study of Thyroid Function Traits Identifies Novel Associations of fT3 With KLF9 and DOT1L.The Journal of clinical endocrinology and metabolism · 2021Pooled it
- Controlled Antenatal Thyroid Screening Study III: Effects of Gestational Thyroid Status on Brain Microstructure.The Journal of clinical endocrinology and metabolism · 2025Trial
- Thyroid hormone supplementation in preterm infants born before 28 weeks gestational age and neurodevelopmental outcome at age 36 months.Thyroid : official journal of the American Thyroid Association · 2014Trial
- Article
- Azetidine-2-carboxylic acid-induced oligodendrogliopathy in vitro and the pathogenesis of multiple sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- Oligodendroglia as Active Immunomodulators in Demyelinating Diseases.Neuroscience bulletin · 2026Review
- Single-nucleus epigenomic profiling of the adult human central nervous system unveils epigenetic memory of developmental programs.Nature neuroscience · 2026Article
- T3 enhances neuronal activity in an induced pluripotent stem cell derived model of early human brain development.European thyroid journal · 2026Article
- Convergent thyroid-ATPase interactions regulate collective behavior in Danionella.Cell reports · 2026Article
- Oral Intake of Plasticizer Di-(2-ethylhexyl) Phthalate Disrupts Cerebellar Myelination via Thyroid Signaling in Aging Mice.Environment & health (Washington, D.C.) · 2025Article
- Human iPSC-Derived Neuron and Oligodendrocyte Co-culture as a Small-Molecule Screening Assay for Myelination.Bio-protocol · 2025Article
- Nuclear hormone receptors control fundamental processes of human fetal neurodevelopment: Basis for endocrine disruption assessment.Environment international · 2025Article
- Implications of Krüppel-like factor signaling in neuroinflammation for neurodegenerative diseases.American journal of translational research · 2025Review
- Article
- Single-Cell Multi-Omics Map of Cell Type-Specific Mechanistic Drivers of Multiple Sclerosis Lesions.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- PAFAH1B3 is a KLF9 target gene that promotes proliferation and metastasis in pancreatic cancer.Scientific reports · 2024Article
- SRF transcriptionally regulates the oligodendrocyte cytoskeleton during CNS myelination.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Gamma entrainment using audiovisual stimuli alleviates chemobrain pathology and cognitive impairment induced by chemotherapy in mice.Science translational medicine · 2024Article
- Article
- Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hypothyroidism is a well-described cause of hypomyelination. In addition, thyroid hormone (T3) has recently been shown to enhance remyelination in various animal models of CNS demyelination. What are the ways in which T3 promotes the development and regeneration of healthy myelin? To begin to understand the mechanisms by which T3 drives myelination, we have identified genes regulated specifically by T3 in purified oligodendrocyte precursor cells (OPCs). Among the genes identified by genomic expression analyses were four transcription factors, Kruppel-like factor 9 (KLF9), basic helix-loop-helix family member e22 (BHLHe22), Hairless (Hr), and Albumin D box-binding protein (DBP), all of which were induced in OPCs by both brief and long term exposure to T3. To begin to investigate the role of these genes in myelination, we focused on the most rapidly and robustly induced of these, KLF9, and found it is both necessary and sufficient to promote oligodendrocyte differentiation in vitro. Surprisingly, we found that loss of KLF9 in vivo negligibly affects the formation of CNS myelin during development, but does significantly delay remyelination in cuprizone-induced demyelinated lesions. These experiments indicate that KLF9 is likely a novel integral component of the T3-driven signaling cascade that promotes the regeneration of lost myelin. Future analyses of the roles of KLF9 and other identified T3-induced genes in myelination may lead to novel insights into how to enhance the regeneration of myelin in demyelinating diseases such as multiple sclerosis.
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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.