ArticleThe Journal of biological chemistry2012
Transforming growth factor-β1 regulates Cdk5 activity in primary sensory neurons.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- Cdk5 modulates orofacial pain through P2X2/3 purinergic receptor-mediated signaling in trigeminal neurons.Frontiers in pharmacology · 2026Article
- Article
- Fascial Pathophysiology in Hypermobility Spectrum Disorders and Hypermobile Ehlers-Danlos Syndrome: A Review of Emerging Evidence.International journal of molecular sciences · 2025Review
- GnRH peripherally modulates nociceptor functions, exacerbating mechanical pain.Frontiers in molecular neuroscience · 2024Article
- Serum Biomarkers of Nociceptive and Neuropathic Pain in Chronic Pancreatitis.The journal of pain · 2023Observational
- The Antinociceptive Effect of Sympathetic Block is Mediated by Transforming Growth Factor β in a Mouse Model of Radiculopathy.Neuroscience bulletin · 2023Article
- Silencing miR-21-5p in sensory neurons reverses neuropathic allodynia via activation of TGF-β-related pathway in macrophages.The Journal of clinical investigation · 2023Article
- Visualization of trigeminal ganglion sensory neuronal signaling regulated by Cdk5.Cell reports · 2022Article
- Effect of TGF-Neural plasticity · 2022Article
- Focusing on cyclin-dependent kinases 5: A potential target for neurological disorders.Frontiers in molecular neuroscience · 2022Review
- Review
- Role of the CXCR4/ALK5/Smad3 Signaling Pathway in Cancer-Induced Bone Pain.Journal of pain research · 2020Article
- A Pathway Analysis Based on Genome-Wide DNA Methylation of Chinese Patients with Graves' Orbitopathy.BioMed research international · 2019Article
- Identifying and Validating Genes with DNA Methylation Data in the Context of Biological Network for Chinese Patients with Graves' Orbitopathy.International journal of endocrinology · 2019Article
- Neuronal Transforming Growth Factor beta Signaling via SMAD3 Contributes to Pain in Animal Models of Chronic Pancreatitis.Gastroenterology · 2018Article
- TNF-α Increases Production of Reactive Oxygen Species through Cdk5 Activation in Nociceptive Neurons.Frontiers in physiology · 2018Article
- Pain improvement in Camurati-Engelmann disease after anti-TNFα therapy.BMJ case reports · 2017Article
- Article
- Effects of TRPC1 on epithelial mesenchymal transition in human airway in chronic obstructive pulmonary disease.Medicine · 2017Article
- Neuroinflammation, Bone Marrow Stem Cells, and Chronic Pain.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In addition to many important roles for Cdk5 in brain development and synaptic function, we reported previously that Cdk5 regulates inflammatory pain signaling, partly through phosphorylation of transient receptor potential vanilloid 1 (TRPV1), an important Na(+)/Ca(2+) channel expressed in primary nociceptive afferent nerves. Because TGF-β regulates inflammatory processes and its receptor is expressed in TRPV1-positive afferents, we studied the cross-talk between these two pathways in sensory neurons during experimental peripheral inflammation. We demonstrate that TGF-β1 increases transcription and protein levels of the Cdk5 co-activator p35 through ERK1/2, resulting in an increase in Cdk5 activity in rat B104 neuroblastoma cells. Additionally, TGF-β1 enhances the capsaicin-induced Ca(2+) influx in cultured primary neurons from dorsal root ganglia (DRG). Importantly, Cdk5 activity was reduced in the trigeminal ganglia and DRG of 14-day-old TGF-β1 knock-out mice, resulting in reduced Cdk5-dependent phosphorylation of TRPV1. The decreased Cdk5 activity is associated with attenuated thermal hyperalgesia in TGF-β1 receptor conditional knock-out mice, where TGF-β signaling is significantly reduced in trigeminal ganglia and DRG. Collectively, our results indicate that active cross-talk between the TGF-β and Cdk5 pathways contributes to inflammatory pain signaling.
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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.