ArticleLife science alliance2021
TrkB signaling regulates the cold-shock protein RBM3-mediated neuroprotection.
Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Molecular mediators of cold adaptation in mammalian cells.Communications biology · 2025Review
- No more nonsense: evaluating poison exons as therapeutic targets in neurodevelopmental disorders.Current opinion in genetics & development · 2025Review
- Therapeutic Hypothermia Increases the Expression of RNA-binding Protein Motif 3 and Attenuates Cognitive Deficits Following Cardiac Arrest in Rats.Neurochemical research · 2025Article
- Therapeutic modulation of protein RBM3 for ischemic stroke treatment.Frontiers in pharmacology · 2025Review
- Single-cell transcriptomics unveils molecular signatures of neuronal vulnerability in a mouse model of prion disease that overlap with Alzheimer's disease.Nature communications · 2024Article
- Cold-shock proteome of myoblasts reveals role of RBM3 in promotion of mitochondrial metabolism and myoblast differentiation.Communications biology · 2024Article
- Mild hypothermia promotes neuronal differentiation of human neural stem cells via RBM3-SOX11 signaling pathway.iScience · 2024Article
- Linking Hypothermia and Altered Metabolism with TrkB Activation.ACS chemical neuroscience · 2023Article
- Hypothermia increases cold-inducible protein expression and improves cerebellar-dependent learning after hypoxia ischemia in the neonatal rat.Pediatric research · 2023Article
- HNRNPH1 regulates the neuroprotective cold-shock protein RBM3 expression through poison exon exclusion.The EMBO journal · 2023Article
- ASO targeting RBM3 temperature-controlled poison exon splicing prevents neurodegeneration in vivo.EMBO molecular medicine · 2023Article
- RNA binding motif protein 3 (RBM3) promotes protein kinase B (AKT) activation to enhance glucose metabolism and reduce apoptosis in skeletal muscle of mice under acute cold exposure.Cell stress & chaperones · 2022Article
- Intracellular Aβ42 Aggregation Leads to Cellular Thermogenesis.Journal of the American Chemical Society · 2022Article
- Associations between RNA-Binding Motif Protein 3, Fibroblast Growth Factor 21, and Clinical Outcome in Patients with Stroke.Journal of clinical medicine · 2022Article
- Hypothermia promotes synaptic plasticity and protective effects in neurological diseases.Brain circulationArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Increasing levels of the cold-shock protein, RNA-binding motif 3 (RBM3), either through cooling or by ectopic over-expression, prevents synapse and neuronal loss in mouse models of neurodegeneration. To exploit this process therapeutically requires an understanding of mechanisms controlling cold-induced RBM3 expression. Here, we show that cooling increases RBM3 through activation of TrkB via PLCγ1 and pCREB signaling. RBM3, in turn, has a hitherto unrecognized negative feedback on TrkB-induced ERK activation through induction of its specific phosphatase, DUSP6. Thus, RBM3 mediates structural plasticity through a distinct, non-canonical activation of TrkB signaling, which is abolished in RBM3-null neurons. Both genetic reduction and pharmacological antagonism of TrkB and its downstream mediators abrogate cooling-induced RBM3 induction and prevent structural plasticity, whereas TrkB inhibition similarly prevents RBM3 induction and the neuroprotective effects of cooling in prion-diseased mice. Conversely, TrkB agonism induces RBM3 without cooling, preventing synapse loss and neurodegeneration. TrkB signaling is, therefore, necessary for the induction of RBM3 and related neuroprotective effects and provides a target by which RBM3-mediated synapse-regenerative therapies in neurodegenerative disorders can be used therapeutically without the need for inducing hypothermia.
Indexed as
Identifiers
What OpenQuestion holds
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.