ArticlePain2009
The c-kit signaling pathway is involved in the development of persistent pain.
Article in Pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- The contribution of stem cell factor and its receptor c-Kit to cancer-induced bone pain.JCI insight · 2026Article
- The Association Between Irritable Bowel Syndrome and Generalized Anxiety Disorder and Influencing Factors: A Mediation Mendelian Randomization Study.Food science & nutrition · 2026Article
- Multifaceted Roles of ALK Family Receptors and Augmentor Ligands in Health and Disease: A Comprehensive Review.Biomolecules · 2023Review
- c-Kit Receptor Maintains Sensory Axon Innervation of the Skin through Src Family Kinases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Development of an AmpliSeqFrontiers in pharmacology · 2018Article
- The Src family kinase inhibitor dasatinib delays pain-related behaviour and conserves bone in a rat model of cancer-induced bone pain.Scientific reports · 2017Article
- Peripheral inflammatory pain sensitisation is independent of mast cell activation in male mice.Pain · 2017Article
- Role of stem cell growth factor/c-Kit in the pathogenesis of irritable bowel syndrome.Experimental and therapeutic medicine · 2017Article
- The impact of inflammatory cells in malignant ascites on small intestinal ICCs' morphology and function.Journal of cellular and molecular medicine · 2015Article
- Molecular signatures of mouse TRPV1-lineage neurons revealed by RNA-Seq transcriptome analysis.The journal of pain · 2014Article
- Epigenetic modification of DRG neuronal gene expression subsequent to nerve injury: etiological contribution to complex regional pain syndromes (Part II).Medical science monitor : international medical journal of experimental and clinical research · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Protein kinase signal transduction pathways play critical roles in regulating nociception. Here we show that c-kit, a tyrosine kinase receptor, is expressed in lamina I and II layer of the dorsal horn. Moreover, the superficial c-kit(+) fibers originate from the dorsal root ganglion, and c-kit in lamina II inner layer comes from intrinsic expression of the spinal cord. Kit(W-v) mice, which contain a hypomorphic mutation, exhibited normal acute pain in most pain behavior tests. In the formalin test, the first phase was not affected, whereas the second phase pain response of Kit(W-v) mice was significantly reduced relative to wild-type littermates. Kit(W-v) mice also showed abnormal neuropathic pain, notably in the contralateral side of nerve injury. The expression and release of CGRP and substance P were not altered by the c-kit mutation. Together, these results implicate c-kit-mediated signal transduction in the development of persistent pain.
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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.