ArticleThe Journal of clinical investigation2013
Chronic itch development in sensory neurons requires BRAF signaling pathways.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
What it found
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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
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- European S2k Guideline on Chronic PruritusActa dermato-venereologica · 2025Guideline
- Mas-Related G-Protein-Coupled Receptors: Emerging Roles in Neuropathic Pain.Biomolecules · 2026Review
- Spinal and supraspinal mechanisms of chronic itch: from neuronal circuits to the neuro-immune-microbial axis.Frontiers in medicine · 2026Review
- Pathophysiologic Mechanisms and Targeted Treatments Associated with the Nervous System in Cutaneous Allergic Diseases.Clinical reviews in allergy & immunology · 2025Review
- Neuronal Mechanisms of Psoriatic Itch: Role of IL-17R/ERK/TRPV4 Signaling Pathway.The Journal of investigative dermatology · 2025Article
- USP45 Represses Melanoma Development by Deubiquitinating and Stabilizing Tumor Suppressor MRGPRF.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A thalamic nucleus reuniens-lateral septum-lateral hypothalamus circuit for comorbid anxiety-like behaviors in chronic itch.Science advances · 2024Article
- The COL6A5-p.Glu2272* mutation induces chronic itch in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Vascular Endothelial Growth Factor a Promotes Chronic Itch via VEGFA-VEGFR2-PI3K-TRPV1 Axis in Allergic Contact Dermatitis.Journal of inflammation research · 2024Article
- 20-HETE mediated TRPV1 activation drives allokinesis via MrgprA3Theranostics · 2024Article
- Mechanisms and treatments of neuropathic itch in a mouse model of lymphoma.The Journal of clinical investigation · 2023Article
- Structures of human gastrin-releasing peptide receptors bound to antagonist and agonist for cancer and itch therapy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Function of gastrin-releasing peptide receptors in ocular itch transmission in the mouse trigeminal sensory system.Frontiers in molecular neuroscience · 2023Article
- Neuronal pentraxin 2 is required for facilitating excitatory synaptic inputs onto spinal neurons involved in pruriceptive transmission in a model of chronic itch.Nature communications · 2022Article
- Pruritus: A Sensory Symptom Generated in Cutaneous Immuno-Neuronal Crosstalk.Frontiers in pharmacology · 2022Review
- Article
- A neuropeptide code for itch.Nature reviews. Neuroscience · 2021Review
- Bombesin-like peptide recruits disinhibitory cortical circuits and enhances fear memories.Cell · 2021Article
- Chemogenetic activation of central gastrin-releasing peptide-expressing neurons elicits itch-related scratching behavior in male and female mice.Pharmacology research & perspectives · 2021Article
- The Role of Transient Receptor Potential A1 and G Protein-Coupled Receptor 39 in Zinc-Mediated Acute and Chronic Itch in Mice.Frontiers in molecular neuroscience · 2021Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Chronic itch, or pruritus, is associated with a wide range of skin abnormalities. The mechanisms responsible for chronic itch induction and persistence remain unclear. We developed a mouse model in which a constitutively active form of the serine/threonine kinase BRAF was expressed in neurons gated by the sodium channel Nav1.8 (BRAF(Nav1.8) mice). We found that constitutive BRAF pathway activation in BRAF(Nav1.8) mice results in ectopic and enhanced expression of a cohort of itch-sensing genes, including gastrin-releasing peptide (GRP) and MAS-related GPCR member A3 (MRGPRA3), in nociceptors expressing transient receptor potential vanilloid 1 (TRPV1). BRAF(Nav1.8) mice showed de novo neuronal responsiveness to pruritogens, enhanced pruriceptor excitability, and heightened evoked and spontaneous scratching behavior. GRP receptor expression was increased in the spinal cord, indicating augmented coding capacity for itch subsequent to amplified pruriceptive inputs. Enhanced GRP expression and sustained ERK phosphorylation were observed in sensory neurons of mice with allergic contact dermatitis– or dry skin–elicited itch; however, spinal ERK activation was not required for maintaining central sensitization of itch. Inhibition of either BRAF or GRP signaling attenuated itch sensation in chronic itch mouse models. These data uncover RAF/MEK/ERK signaling as a key regulator that confers a subset of nociceptors with pruriceptive properties to initiate and maintain long-lasting itch sensation.
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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.