PainPrint maps gene expression across dorsal root ganglion neuron subtypes to uncover the cellular basis of pain sensitivity — at single-cell resolution.
Interactive visualization of 990 DRG neurons. Click any cluster to explore cell identity and pain relevance.
Search any pain gene — see expression across all 10 subtypes with anatomical body map and mechanistic annotations.
Differential expression reveals which genes are upregulated in chronic pain states across neuron subtypes.
Enter a pain condition — see the implicated genes, cell types, and anatomical pathway highlighted on a body map.
UMAP projection of 990 dorsal root ganglion cells — click a cluster to view cell type details
Represents the largest source of variation in gene expression across all cells. Cells with similar transcriptomic profiles cluster together along this axis. No direct biological meaning — position only reflects relative similarity.
Captures the second largest source of variation, orthogonal to UMAP 1. Together, UMAP 1 and 2 compress 18-dimensional gene expression data into 2D space — preserving local neighborhood structure so that clusters reflect real biological cell-type differences.
Select any point on the UMAP to view cell type information, marker genes, and pain relevance.
Search a pain-related gene to view its expression across DRG cell types
Select a gene to view expression details
Select a gene to see its action sites
Enter a pain location or condition to explore the underlying genes and cell types
Data sources, methods, and scientific rationale
PainPrint is an interactive single-cell transcriptomic atlas exploring the cellular and molecular basis of pain. The platform maps gene expression across dorsal root ganglion (DRG) neuron subtypes to identify which cell populations and genetic programs underlie differences in pain sensitivity.
The central question: Why do people experience pain so differently? Emerging evidence from single-cell transcriptomics suggests that the answer lies in the molecular heterogeneity of sensory neuron subtypes — and how inflammation, injury, or genetic variation shifts gene expression within those subtypes.
"Which dorsal root ganglion cell types and pain-associated genes show the greatest transcriptional changes in chronic pain states, and how do their expression patterns relate to known neurobiological mechanisms?"
This platform integrates cell-type identity, gene expression, anatomical localization, and differential expression to provide a mechanistic view of pain at single-cell resolution.
GSE59739_DataTable.txt.gz retrieved from NCBI GEO FTP. Rows = genes, columns = cells; cell metadata encoded in column names.
Content == "cell" (n = 799 single cells), excluding bulk controls and empty wells.
| Cell Type | Class | n cells | Key defining markers |
|---|---|---|---|
| NF1 (Aβ RA-LTMR) | NF | 28 | Nefh+, Necab2+ |
| NF2 (Aβ SA-LTMR) | NF | 15 | Nefh+, Hapln4+ |
| NF3 (Aδ-HTMR) | NF | 211 | Nefh+, moderate Trpv1 |
| NF4 (proprioceptor) | NF | 88 | Nefh+, Pvalb+ |
| PEP1 (peptidergic) | PEP | 83 | Calca+, moderate Tac1 |
| PEP2 (peptidergic) | PEP | 176 | Tac1 high > Calca |
| NP1 (non-peptidergic) | NP | 95 | Mrgprd+ |
| NP2 (non-peptidergic) | NP | 94 | Low all markers, small-diameter |
| NP3 (non-peptidergic) | NP | 3 | Nppb+ |
| Satellite Glia | Glia | 91 | Fabp7+ |
Raw data publicly available from NCBI GEO under accession GSE59739. Data redistributed under CC0 / public domain per GEO terms. NP1 (n=1) merged with NP2 (n=94) via weighted average for statistical stability.
DRG neurons are classified into three major classes based on myelination, function, and molecular markers:
⚠️ Gene expression values shown are illustrative, derived from published DRG single-cell datasets and curated literature. They are intended for educational and exploratory purposes, not for clinical interpretation.
⚠️ The Pain vs Control differential expression reflects patterns observed in chronic pain animal models. Human chronic pain transcriptomics may differ.
⚠️ Body map annotations represent the primary anatomical sites of gene action based on current literature and may not capture all expression contexts.
⚠️ This platform is an independent academic project and is not affiliated with any clinical institution.
Differential gene expression between chronic pain and control conditions in peptidergic nociceptors