ArticleBMC biology2017
Smad4 SUMOylation is essential for memory formation through upregulation of the skeletal myopathy gene TPM2.
Article in BMC biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- PIAS1-mediated GSK3β SUMOylation exacerbates tauopathy and cognitive deficits in Alzheimer's disease models.Molecular psychiatry · 2026Article
- The ubiquitin-proteasome system and learning-dependent synaptic plasticity - A 10 year update.Neuroscience and biobehavioral reviews · 2023Review
- Protein SUMOylation is a sex-specific regulator of fear memory formation in the amygdala.Behavioural brain research · 2022Article
- Neuroadaptations and TGF-β signaling: emerging role in models of neuropsychiatric disorders.Molecular psychiatry · 2022Review
- Integrative Analysis Extracts a Core ceRNA Network of the Fetal Hippocampus With Down Syndrome.Frontiers in genetics · 2020Article
- Galectin-3 promotes Aβ oligomerization and Aβ toxicity in a mouse model of Alzheimer's disease.Cell death and differentiation · 2020Article
- Protein inhibitor of activated STAT1 SerBritish journal of pharmacology · 2019Article
- Genetic heterogeneity of Alzheimer's disease in subjects with and without hypertension.GeroScience · 2019Article
- Review
- Comprehensive Analysis of lncRNA-miRNA- mRNA Network Ascertains Prognostic Factors in Patients with Colon Cancer.Technology in cancer research & treatmentArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSmad4 is a critical effector of TGF-β signaling that regulates a variety of cellular functions. However, its role in the brain has rarely been studied. Here, we examined the molecular mechanisms underlying the post-translational regulation of Smad4 function by SUMOylation, and its role in spatial memory formation.
resultsIn the hippocampus, Smad4 is SUMOylated by the E3 ligase PIAS1 at Lys-113 and Lys-159. Both spatial training and NMDA injection enhanced Smad4 SUMOylation. Inhibition of Smad4 SUMOylation impaired spatial learning and memory in rats by downregulating TPM2, a gene associated with skeletal myopathies. Similarly, knockdown of TPM2 expression impaired spatial learning and memory, while TPM2 mRNA and protein expression increased after spatial training. Among the TPM2 mutations associated with skeletal myopathies, the TPM2E122K mutation was found to reduce TPM2 expression and impair spatial learning and memory in rats.
conclusionsWe have identified a novel role of Smad4 SUMOylation and TPM2 in learning and memory formation. These results suggest that patients with skeletal myopathies who carry the TPM2E122K mutation may also have deficits in learning and memory functions.
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