ArticleProceedings of the National Academy of Sciences of the United States of America2011
Nontelomeric splice variant of telomere repeat-binding factor 2 maintains neuronal traits by sequestering repressor element 1-silencing transcription factor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- RNArchitects: how hnRNPs shape neuronal landscapes.Brain : a journal of neurology · 2026Review
- Cannabinol's Modulation of Genes Involved in Oxidative Stress Response and Neuronal Plasticity: A Transcriptomic Analysis.Antioxidants (Basel, Switzerland) · 2025Article
- Role of the telomeric factor TRF2 in post-hypoxic brain damages.Redox biology · 2024Article
- Telomeres expand sphere of influence: emerging molecular impact of telomeres in non-telomeric functions.Trends in genetics : TIG · 2023Review
- Connecting telomere maintenance and regulation to the developmental origin and differentiation states of neuroblastoma tumor cells.Journal of hematology & oncology · 2022Review
- The non-telomeric evolutionary trajectory of TRF2 in zebrafish reveals its specific roles in neurodevelopment and aging.Nucleic acids research · 2022Article
- Reciprocal impacts of telomerase activity and ADRN/MES differentiation state in neuroblastoma tumor biology.Communications biology · 2021Article
- The Intra- and Extra-Telomeric Role of TRF2 in the DNA Damage Response.International journal of molecular sciences · 2021Review
- Human telomerase is directly regulated by non-telomeric TRF2-G-quadruplex interaction.Cell reports · 2021Article
- Extra-telomeric impact of telomeres: Emerging molecular connections in pluripotency or stemness.The Journal of biological chemistry · 2020Review
- TRF2 positively regulates SULF2 expression increasing VEGF-A release and activity in tumor microenvironment.Nucleic acids research · 2019Article
- Non-coding RNA inNon-coding RNA research · 2018Review
- Identification and characterization of two novel alternatively spliced E2F1 transcripts in the rat CNS.Molecular and cellular neurosciences · 2018Article
- The differential spatiotemporal expression pattern of shelterin genes throughout lifespan.Aging · 2017Article
- SIRT6 interacts with TRF2 and promotes its degradation in response to DNA damage.Nucleic acids research · 2017Article
- The long and the short of TRF2 in neurogenesis.Cell cycle (Georgetown, Tex.) · 2016Review
- G-quadruplex RNA binding and recognition by the lysine-specific histone demethylase-1 enzyme.RNA (New York, N.Y.) · 2016Article
- Alternative Splicing of Neuronal Differentiation Factor TRF2 Regulated by HNRNPH1/H2.Cell reports · 2016Article
- The new (dis)order in RNA regulation.Cell communication and signaling : CCS · 2016Review
- Novel RNA- and FMRP-binding protein TRF2-S regulates axonal mRNA transport and presynaptic plasticity.Nature communications · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Telomere repeat-binding factor 2 (TRF2) is critical for telomere integrity in dividing stem and somatic cells, but its role in postmitotic neurons is unknown. Apart from protecting telomeres, nuclear TRF2 interacts with the master neuronal gene-silencer repressor element 1-silencing transcription factor (REST), and disruption of this interaction induces neuronal differentiation. Here we report a developmental switch from the expression of TRF2 in proliferating neural progenitor cells to expression of a unique short nontelomeric isoform of TRF2 (TRF2-S) as neurons establish a fully differentiated state. Unlike nuclear TRF2, which enhances REST-mediated gene repression, TRF2-S is located in the cytoplasm where it sequesters REST, thereby maintaining the expression of neuronal genes, including those encoding glutamate receptors, cell adhesion, and neurofilament proteins. In neurons, TRF2-S-mediated antagonism of REST nuclear activity is greatly attenuated by either overexpression of TRF2 or administration of the excitatory amino acid kainic acid. Overexpression of TRF2-S rescues kainic acid-induced REST nuclear accumulation and its gene-silencing effects. Thus, TRF2-S acts as part of a unique developmentally regulated molecular switch that plays critical roles in the maintenance and plasticity of neurons.
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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.