ArticleFrontiers in neuroscience2011
Elk-1 a transcription factor with multiple facets in the brain.
Article in Frontiers in neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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Who cites it
116 citing papers in PubMed, 196 citations in OpenAlex.
- Trial
- Integrating short-read and long-read single-cell transcriptomics of pig pituitary reveals mechanisms of high-altitude hypoxia adaptation.PLoS genetics · 2026Article
- TNF-α-Induced Upregulation of ADAMTS-8 Expression in SW480 Cells: Implications for Intracellular Signaling Pathways and Transcription Factor Activity.Cell biochemistry and biophysics · 2026Article
- Synaptic potentiation requires PARP1 activation: prevailing concepts are revisited.Molecular psychiatry · 2026Review
- Targeting neuroplasticity in old brain: restoring synapse with cognitive strategies.Biogerontology · 2026Review
- Transcription factors implicated in substance use disorder, from immediate early genes to altered gene expression.Brain research · 2026Review
- miR-2110 orchestrates ERK-ELK1 transcriptional repression to induce cell-cycle arrest and enhance cytarabine sensitivity in acute myeloid leukemia.Frontiers in oncology · 2026Article
- TDP-43 loss induces cryptic polyadenylation in ALS/FTD.Nature neuroscience · 2025Article
- Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review.Cells · 2025Review
- Proteomic Investigation of Neurotrophic trans-Banglene Reveals Potential Link to Iron Homeostasis.Molecular neurobiology · 2025Article
- Massively parallel reporter assays and mouse transgenic assays provide correlated and complementary information about neuronal enhancer activity.Nature communications · 2025Article
- Human genetic variation determines 24-hour rhythmic gene expression and disease risk.Nature communications · 2025Article
- Virally mediated expression of a biologically active peptide to restrain the nuclear functions of ERK1/2 attenuates learning extinction but not acquisition.Molecular brain · 2025Article
- Interpretable AI for inference of causal molecular relationships from omics data.Science advances · 2025Article
- ELK1 regulates BMPR1B transcriptional activity in ovine granulosa cells.Frontiers in cell and developmental biology · 2025Article
- Activity-dependent transcriptional programs in memory regulate motor recovery after stroke.Communications biology · 2024Article
- Exosomal lncRNA HCP5 derived from human bone marrow mesenchymal stem cells improves chronic periodontitis by miR-24-3p/Heliyon · 2024Article
- Protein Kinase A in neurological disorders.Journal of neurodevelopmental disorders · 2024Review
- BRCA1 and ELK-1 regulate neural progenitor cell fate in the optic tectum in response to visual experience inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Transcription factors regulating vasculogenesis and angiogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
56 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ternary complex factor (TCF) Elk-1 is a transcription factor that regulates immediate early gene (IEG) expression via the serum response element (SRE) DNA consensus site. Elk-1 is associated with a dimer of serum response factor (SRF) at the SRE site, and its phosphorylation occurs at specific residues in response to mitogen-activated protein kinases (MAPKs), including c-Jun-N terminal kinase (JNK), p38/MAPK, and extracellular-signal regulated kinase (ERK). This phosphorylation event is critical for triggering SRE-dependent transcription. Although MAPKs are fundamental actors for the instatement and maintenance of memory, and much investigation of their downstream signaling partners have been conducted, no data yet clearly implicate Elk-1 in these processes. This is partly due to the complexity of Elk-1 sub-cellular localization, and hence functions, within neurons. Elk-1 is present in its resting state in the cytoplasm, where it colocalizes with mitochondrial proteins or microtubules. In this particular sub-cellular compartment, overexpression of Elk-1 is toxic for neuronal cells. When phosphorylated by the MAPK/ERK, Elk-1 translocates to the nucleus where it is implicated in regulating chromatin remodeling, SRE-dependent transcription, and neuronal differentiation. Another post-translational modification is the conjugation to SUMO (Small Ubiquitin-like MOdifier), which relocalizes Elk-1 in the cytoplasm. Thus, Elk-1 plays a dual role in neuronal functions: pro-apoptotic within the cytoplasm, and pro-differentiation within the nucleus. To address the role of Elk-1 in the brain, one must be aware of its multiple facets, and design molecular tools that will shut down Elk-1 expression, trafficking, or activation, in specific neuronal compartments. We summarize in this review the known molecular functions of Elk-1, its regulation in neuronal cells, and present evidence of its possible implication in model systems of synaptic plasticity, learning, but also in neurodegenerative diseases.
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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 Socratic graph.