ArticleMolecular and cellular biology2015
LIMK1 regulates long-term memory and synaptic plasticity via the transcriptional factor CREB.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 76 citations in OpenAlex.
- Modeling Williams syndrome from a neurodevelopmental perspective: recent advances, model-based translational insights and future directions.World journal of pediatrics : WJP · 2026Review
- Native Taylor/Non-Taylor Dispersion-Mass Spectrometry (TNT-MS) Allows Rapid Protein Desalting and Multiplexed, Label-Free Ligand Screening.Small methods · 2026Article
- Protective role of high-intensity exercise and lactate against sleep deprivation-induced alterations in hippocampal gene expression and spatial learning.Neuroscience applied · 2026Article
- LIMK1 Deficiency Disrupts Hippocampal-Cortical Memory Consolidation and Attenuates Trauma-Induced PTSD-like Behavior.Biology · 2025Article
- Review
- Role of LIMK1-cofilin-actin axis in dendritic spine dynamics in Alzheimer's disease.Cell death & disease · 2025Review
- Regulation and signaling of the LIM domain kinases.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Article
- Engineering memory with an extrinsically disordered kinase.Science advances · 2023Article
- Hippocampal LIMK1-mediated Structural Synaptic Plasticity in Neurobehavioral Deficits Induced by a Low-dose Heavy Metal Mixture.Molecular neurobiology · 2023Article
- Dorsal visual stream and LIMK1: hemideletion, haplotype, and enduring effects in children with Williams syndrome.Journal of neurodevelopmental disorders · 2023Article
- LIM Kinases, LIMK1 and LIMK2, Are Crucial Node Actors of the Cell Fate: Molecular to Pathological Features.Cells · 2023Review
- Repetitive transcranial magnetic stimulation promotes neurological functional recovery in rats with traumatic brain injury by upregulating synaptic plasticity-related proteins.Neural regeneration research · 2023Article
- Mahonia Alkaloids (MA) Ameliorate Depression Induced Gap Junction Dysfunction by miR-205/Cx43 Axis.Neurochemical research · 2022Article
- Decoding brain memory formation by single-cell RNA sequencing.Briefings in bioinformatics · 2022Article
- Review
- LIMK1 Interacts with STK25 to Regulate EMT and Promote the Proliferation and Metastasis of Colorectal Cancer.Journal of oncology · 2022Article
- Inhibition of Rac1 in ventral hippocampal excitatory neurons improves social recognition memory and synaptic plasticity.Frontiers in aging neuroscience · 2022Article
- Rho-associated kinases contribute to the regulation of tau phosphorylation and amyloid metabolism during neuronal plasticity.Pharmacological reports : PR · 2021Article
- Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Deletion of the LIMK1 gene is associated with Williams syndrome, a unique neurodevelopmental disorder characterized by severe defects in visuospatial cognition and long-term memory (LTM). However, whether LIMK1 contributes to these deficits remains elusive. Here, we show that LIMK1-knockout (LIMK1(-/-)) mice are drastically impaired in LTM but not short-term memory (STM). In addition, LIMK1(-/-) mice are selectively defective in late-phase long-term potentiation (L-LTP), a form of long-lasting synaptic plasticity specifically required for the formation of LTM. Furthermore, we show that LIMK1 interacts and regulates the activity of cyclic AMP response element-binding protein (CREB), an extensively studied transcriptional factor critical for LTM. Importantly, both L-LTP and LTM deficits in LIMK1(-/-) mice are rescued by increasing the activity of CREB. These results provide strong evidence that LIMK1 deletion is sufficient to lead to an LTM deficit and that this deficit is attributable to CREB hypofunction. Our study has identified a direct gene-phenotype link in mice and provides a potential strategy to restore LTM in patients with Williams syndrome through the enhancement of CREB activity in the adult brain.
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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 OpenQuestion graph.