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IL32
IL32
Overview
<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">il32</th>
</tr>
<tr>
<td class="label">gene = IL32</td>
<td>name = Interleukin 32</td>
</tr>
<tr>
<td class="label">ncbi_gene_id = 9235</td>
<td>ensembl = ENSG00000127124</td>
</tr>
<tr>
<td class="label">Partner</td>
<td>Interaction Type</td>
</tr>
<tr>
<td class="label">TNFR1/2</td>
<td>Receptor binding</td>
</tr>
<tr>
<td class="label">IL-6R</td>
<td>Cytokine cross-talk</td>
</tr>
<tr>
<td class="label">PKR</td>
<td>Apoptosis induction</td>
</tr>
<tr>
<td class="label">TLR3</td>
<td>Viral recognition</td>
</tr>
<tr>
<td class="label">Caspase-1</td>
<td>Inflammasome</td>
</tr>
<tr>
<td class="label">Approach</td>
<td>Mechanism</td>
</tr>
<tr>
<td class="label">Anti-IL-32 antibodies</td>
<td>Neutralize IL-32 activity</td>
</tr>
<tr>
<td class="label">IL-32 isoforms selective targeting</td>
<td>Target specific variants</td>
</tr>
<tr>
<td class="label">Downstream pathway inhibitors</td>
<td>Block NF-κB, MAPK</td>
</tr>
<tr>
<td class="label">Cell-penetrant inhibitors</td>
<td>Intracellular targeting</td>
</tr>
<tr>
<td class="label">Gene therapy</td>
<td>Modulate expression</td>
</tr>
<tr>
<td class="label">Receptor</td>
<td>Multiple</td>
</tr>
<tr>
<td class="label">Signaling</td>
<td>NF-κB, MAPK, PKR</td>
</tr>
<tr>
<td class="label">CNS expression</td>
<td>Neurons, g...
IL32
Overview
<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">il32</th>
</tr>
<tr>
<td class="label">gene = IL32</td>
<td>name = Interleukin 32</td>
</tr>
<tr>
<td class="label">ncbi_gene_id = 9235</td>
<td>ensembl = ENSG00000127124</td>
</tr>
<tr>
<td class="label">Partner</td>
<td>Interaction Type</td>
</tr>
<tr>
<td class="label">TNFR1/2</td>
<td>Receptor binding</td>
</tr>
<tr>
<td class="label">IL-6R</td>
<td>Cytokine cross-talk</td>
</tr>
<tr>
<td class="label">PKR</td>
<td>Apoptosis induction</td>
</tr>
<tr>
<td class="label">TLR3</td>
<td>Viral recognition</td>
</tr>
<tr>
<td class="label">Caspase-1</td>
<td>Inflammasome</td>
</tr>
<tr>
<td class="label">Approach</td>
<td>Mechanism</td>
</tr>
<tr>
<td class="label">Anti-IL-32 antibodies</td>
<td>Neutralize IL-32 activity</td>
</tr>
<tr>
<td class="label">IL-32 isoforms selective targeting</td>
<td>Target specific variants</td>
</tr>
<tr>
<td class="label">Downstream pathway inhibitors</td>
<td>Block NF-κB, MAPK</td>
</tr>
<tr>
<td class="label">Cell-penetrant inhibitors</td>
<td>Intracellular targeting</td>
</tr>
<tr>
<td class="label">Gene therapy</td>
<td>Modulate expression</td>
</tr>
<tr>
<td class="label">Receptor</td>
<td>Multiple</td>
</tr>
<tr>
<td class="label">Signaling</td>
<td>NF-κB, MAPK, PKR</td>
</tr>
<tr>
<td class="label">CNS expression</td>
<td>Neurons, glia</td>
</tr>
<tr>
<td class="label">Therapeutic targeting</td>
<td>Emerging</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td><a href="/wiki/inflammation" style="color:#ef9a9a">Inflammation</a>, <a href="/wiki/psoriasis" style="color:#ef9a9a">Psoriasis</a></td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">17 edges</a></td>
</tr>
</table>
IL32
{{ infobox .infobox-gene
| gene = IL32
| name = Interleukin 32
| chromosome = 16p13.3
| ncbi_gene_id = 9235
| ensembl = ENSG00000127124
| uniprot = P24001
| gene_family = IL-32 cytokine family
| diseases = Rheumatoid Arthritis, Inflammatory Disorders, Alzheimer's Disease, Parkinson's Disease, Multiple Sclerosis
}}
Introduction
IL32 (Interleukin 32) is a pro-inflammatory cytokine originally identified based on its elevated expression in activated natural killer (NK) cells and T cells [1/https://pubmed.ncbi.nlm.nih.gov/15816860/). Unlike typical interleukins, IL32 is a highly basic, heparin-binding protein that lacks the conventional cytokine structure.[@a2021] Instead, it adopts a unique three-dimensional fold that allows it to interact with multiple receptors and cell types. IL32 is now recognized as a potent mediator of inflammation in various diseases, including rheumatoid arthritis, inflammatory bowel disease, and potentially neurodegenerative diseases [2/https://pubmed.ncbi.nlm.nih.gov/12885573/).
The cytokine is expressed in various cell types including T cells, NK cells, monocytes, epithelial cells, and endothelial cells. More importantly, recent studies have detected IL32 expression in the central nervous system (CNS), where it may contribute to neuroinflammation and disease pathogenesis [8/https://pubmed.ncbi.nlm.nih.gov/22572556/). Given the central role of neuroinflammation in neurodegenerative diseases, IL32 represents a potentially important link between peripheral immune responses and CNS pathology.[@h2022]
Gene and Protein Structure
Genomic Organization
The IL32 gene is located on chromosome 16p13.3 and encodes multiple protein isoforms through alternative splicing. The human IL32 gene produces at least eight isoforms (IL32α, β, γ, δ, ε, ζ, η, and θ), each with distinct biological activities and expression patterns.
Protein Architecture
The IL32 protein exhibits several unique features [1](https://pubmed.ncbi.nlm.nih.gov/15816860/):
- Unique fold: Unlike typical cytokines, IL32 has a distinct structure without the classic four-helix bundle
- Heparin binding: Basic residues allow binding to heparin sulfate proteoglycans
- Multiple isoforms: Alternative splicing generates diverse protein variants
- Secreted and intracellular forms: Can function both extracellularly and within cells
- Proline-rich regions: Important for protein-protein interactions
Expression Pattern
Peripheral Expression
IL32 is expressed in various peripheral tissues and cell types:
- T lymphocytes: Activated CD4+ and CD8+ T cells
- Natural killer cells: NK cell activation induces IL32
- Monocytes/macrophages: Pro-inflammatory signaling
- Epithelial cells: Skin, lung, intestinal epithelium
- Endothelial cells: Vascular endothelial cells
Brain Expression
In the CNS, IL32 expression has been documented in [8](https://pubmed.ncbi.nlm.nih.gov/22572556/):
- Neurons: Various brain regions including cortex and hippocampus
- Astrocytes: Reactive astrocytes under inflammatory conditions
- Microglia: Activated microglial cells
- Endothelial cells: Of the blood-brain barrier
Function and Mechanism
Signaling Pathways
IL32 activates multiple signaling cascades [3](https://pubmed.ncbi.nlm.nih.gov/16502434/):
Biological Activities
IL32 exhibits multiple functions [5](https://pubmed.ncbi.nlm.nih.gov/20383177/):
- Pro-inflammatory cytokine: Induces other inflammatory cytokines (TNF-α, IL-1β, IL-6)
- Cell adhesion: Promotes monocyte and neutrophil adhesion
- Anti-viral response: Induced by viral infections
- Apoptosis induction: Through PKR activation
- Cell proliferation: Context-dependent effects
Disease Associations
Rheumatoid Arthritis
IL32 is highly expressed in rheumatoid arthritis (RA) and contributes to disease pathogenesis [2](https://pubmed.ncbi.nlm.nih.gov/12885573/) [26](https://pubmed.ncbi.nlm.nih.gov/26853558/):
- Synovial fluid IL-32 levels correlate with disease severity
- IL-32 induces pro-inflammatory cytokines in synovial fibroblasts
- Animal models show IL-32 drives joint inflammation
Alzheimer's Disease
In [Alzheimer's disease)(/diseases/alzheimer-disease), IL32 may contribute through [9/https://pubmed.ncbi.nlm.nih.gov/16876765/):
Neuroinflammation: Elevated IL-32 in AD brains may amplify inflammatory responses
Microglial Activation: IL-32 can activate microglia, promoting chronic inflammation [11/https://pubmed.ncbi.nlm.nih.gov/26284489/) [12/https://pubmed.ncbi.nlm.nih.gov/22801412/)
TREM2 Interaction: IL-32 signaling may intersect with TREM2 pathways important in AD microglia [10](https://pubmed.ncbi.nlm.nih.gov/29453415/)
Parkinson's Disease
In [Parkinson's disease)(/diseases/parkinsons-disease), IL32 may contribute to:
- Chronic neuroinflammation in substantia nigra
- Activation of microglia surrounding dopaminergic neurons
- Enhancement of inflammatory responses to α-synuclein
Multiple Sclerosis
IL32 is implicated in [multiple sclerosis](/diseases/multiple-sclerosis) [9/https://pubmed.ncbi.nlm.nih.gov/24286046/):
- Elevated in MS lesions and cerebrospinal fluid
- Contributes to demyelination and inflammation
- Animal model studies show involvement in EAE
Role in Neurodegeneration
Neuroinflammation
Chronic neuroinflammation is a hallmark of neurodegenerative diseases [12/https://pubmed.ncbi.nlm.nih.gov/22801412/), and IL32 contributes through multiple mechanisms:
Aging Effects
Aging-related changes in cytokine expression contribute to neurodegeneration [13](https://pubmed.ncbi.nlm.nih.gov/22155375/):
- Immunosenescence alters IL-32 responses
- Chronic low-grade inflammation increases with age
- Microglial priming makes neurons more vulnerable
Molecular Pathway: IL-32 in Neuroinflammation
Interaction Network
IL32 participates in several molecular interactions:
Research and Clinical Significance
Therapeutic Targeting
IL32 represents a potential therapeutic target [25/https://pubmed.ncbi.nlm.nih.gov/27429039/):
- Neutralizing antibodies: Block IL-32 signaling
- Small molecule inhibitors: Target downstream pathways
- Soluble receptors: Decoy receptors
- Gene therapy: Modulate expression
Biomarker Potential
IL32 may serve as:
- Marker of inflammatory status
- Disease progression indicator
- Therapeutic response monitor
Summary
IL32 is a unique pro-inflammatory cytokine with important roles in immune regulation and inflammation. Its expression in the CNS and contribution to neuroinflammation make it relevant to neurodegenerative disease pathogenesis. The cytokine's ability to amplify inflammatory responses through multiple pathways suggests it may be an important therapeutic target for conditions like Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Further research into IL32's specific roles in neurodegeneration may reveal novel therapeutic opportunities.
Detailed Signaling Mechanisms
Receptor Interactions and Signal Initiation
IL-32 signals through multiple receptor interactions, though its precise receptor(s) remain under investigation [3/https://pubmed.ncbi.nlm.nih.gov/16502434/). Current evidence suggests IL-32 can engage:
Primary receptor candidates:
- Proteinase-activated receptor 2 (PAR2): IL-32 has been shown to activate PAR2, triggering NF-κB and MAPK signaling cascades
- TNF receptors: IL-32 can interact with TNFR1 and TNFR2, leveraging the broader TNF signaling network
- Integrin interactions: Heparin-binding properties allow interaction with cell surface proteoglycans and integrins
The diversity of receptor interactions explains IL-32's pleiotropic effects across different cell types and disease contexts.
Intracellular Signaling Cascades
Upon receptor engagement, IL-32 activates multiple intracellular pathways 3/https://pubmed.ncbi.nlm.nih.gov/16502434/):
NF-κB Pathway:
MAPK Pathways:
- p38 MAPK: Involved in cytokine production, cell survival, and stress responses
- JNK pathway: Regulates apoptosis and inflammatory gene expression
- ERK1/2 pathway: Controls cell proliferation and differentiation
- Double-stranded RNA-dependent protein kinase (PKR) can be activated by IL-32
- Leads to eIF2α phosphorylation and translational arrest
- Triggers intrinsic apoptotic pathways through mitochondrial dysfunction
Inflammasome Activation
IL-32 can activate caspase-1 through inflammasome formation:
- NLRP3 inflammasome assembly in response to IL-32 signaling
- Processing of pro-IL-1β and pro-IL-18 to mature forms
- Pyroptosis induction in extreme cases
- Amplification of inflammatory responses
IL-32 in Alzheimer's Disease
Amyloid Relationship
IL-32 shows complex interactions with amyloid-beta (Aβ) pathology in Alzheimer's disease [9/https://pubmed.ncbi.nlm.nih.gov/16876765/):
Aβ-Induced IL-32:
- Aβ peptides can directly stimulate IL-32 production in microglia
- IL-32 levels correlate with plaque burden in animal models
- IL-32 may represent a bridge between amyloid pathology and neuroinflammation
- Potential modulation of APP processing through NF-κB
- Influence on amyloid clearance mechanisms
- Effects on microglial phagocytosis
Tau Pathology Connection
IL-32 may influence tau phosphorylation and spread:
- NF-κB activation can modulate kinase expression
- Effects on tau propagation mechanisms
- Contribution to spreading pathology
Synaptic Dysfunction
IL-32 contributes to synaptic pathology in AD [12/https://pubmed.ncbi.nlm.nih.gov/22801412/):
- Pro-inflammatory milieu disrupts synaptic plasticity
- Cytokine-induced changes in glutamate signaling
- Direct effects on dendritic spine morphology
- Contribution to early memory deficits
Microglial TREM2 Interactions
The TREM2 variant in AD critically affects microglial responses to IL-32 [10/https://pubmed.ncbi.nlm.nih.gov/29453415/):
- TREM2 signaling modulates IL-32-induced cytokine production
- Altered microglial phenotype in AD affects IL-32 responses
- Impaired amyloid clearance in the presence of IL-32
- Potential for therapeutic targeting of the IL-32/TREM2 axis
IL-32 in Parkinson's Disease
Dopaminergic Neuron Vulnerability
In Parkinson's disease, IL-32 contributes to the selective vulnerability of dopaminergic neurons [12](https://pubmed.ncbi.nlm.nih.gov/22801412/):
- Chronic neuroinflammation in the substantia nigra
- IL-32 expression in proximity to surviving neurons
- Contribution to progressive neuronal loss
α-Synuclein Interactions
IL-32 may interact with α-synuclein pathology:
- Modulation of microglial responses to α-synuclein
- Potential effects on aggregation and clearance
- Role in spreading pathology
LRRK2 Connections
Given LRRK2's importance in PD:
- IL-32 signaling may intersect with LLRK2 pathways
- Microglial activation states affected by both
- Potential for combined therapeutic targeting
IL-32 in Multiple Sclerosis
Demyelination and Remyelination
IL-32 plays complex roles in MS pathogenesis [9](https://pubmed.ncbi.nlm.nih.gov/24286046/):
In demyelination:
- Promotes inflammatory demyelination in EAE models
- Contributes to oligodendrocyte damage
- Enhances immune cell recruitment to lesions
- May impair remyelination efficiency
- Chronic inflammation interferes with repair
- Therapeutic targeting could enhance recovery
Blood-Brain Barrier
IL-32 affects BBB integrity [15](https://pubmed.ncbi.nlm.nih.gov/22884190/):
- Increases BBB permeability
- Promotes immune cell infiltration
- Contributes to lesion formation
Animal Models
EAE Model
Experimental autoimmune encephalomyelitis (EAE) provides insights:
- IL-32 expression increases during disease
- Neutralization reduces disease severity
- Therapeutic targeting is feasible
Transgenic Models
Current models include:
- IL-32 overexpression mice
- IL-32 knockout mice
- Humanized models for translational studies
Limitations and Future Directions
Current model limitations:
- Species differences in IL-32 biology
- Need for CNS-specific knockouts
- Development of better PD models
Therapeutic Development
Current Strategies
Several approaches are being explored [25](https://pubmed.ncbi.nlm.nih.gov/27429039/):
Challenges
Key obstacles to therapeutic development:
- Complexity of cytokine networks
- BBB penetration requirements
- Patient selection biomarkers
- Timing of intervention
Combination Approaches
Future strategies may include:
- IL-32 targeting with anti-inflammatory agents
- Combination with disease-modifying therapies
- Personalized approaches based on IL-32 status
Biomarker Potential
Diagnostic Applications
IL-32 may serve as:
- Peripheral biomarker for neuroinflammation
- CSF marker for disease activity
- Imaging correlation for neuroinflammation load
Prognostic Value
Prognostic applications include:
- Disease progression indicators
- Treatment response monitoring
- Risk stratification
Monitoring Applications
Therapeutic monitoring potential:
- Pharmacodynamic markers
- Dose optimization guides
- Relapse prediction
Comparative Cytokine Analysis
IL-32 vs Other Pro-inflammatory Cytokines
Functional Relationships
IL-32 interacts with other cytokines:
- Amplifies IL-1β and TNF-α responses
- Synergizes with IL-6 in inflammation
- Modulates anti-inflammatory cytokines
Research Methods
Detection and Quantification
Current methodologies include:
- ELISA for protein detection
- qPCR for mRNA analysis
- Immunohistochemistry for localization
- Single-cell RNA-seq for cell-type specificity
Functional Studies
Experimental approaches:
- Recombinant IL-32 treatment
- Knockdown/knockout studies
- Reporter assays for signaling
- Primary cell culture models
Clinical Studies
Human research approaches:
- Cross-sectional patient studies
- Longitudinal cohort studies
- Intervention trials
- Biomarker validation
Future Directions
Key Research Questions
Critical gaps in knowledge:
Emerging Approaches
New research directions:
- Cryo-EM for structural insights
- Single-cell resolution studies
- Systems immunology approaches
- Machine learning for pattern discovery
Clinical Translation Priorities
Translation priorities:
- Biomarker development
- Patient stratification
- Combination therapy design
- Prevention strategies
References (Continued)
Genetics and Population Studies
IL32 Gene Variants
The IL32 gene shows polymorphism across populations:
- Multiple SNPs identified in coding and non-coding regions
- Some variants associated with disease susceptibility
- Population-specific allele frequencies
Association Studies
Genetic studies have examined IL32 variants:
- Rheumatoid arthritis associations replicated
- Inflammatory bowel disease links identified
- Neurodegenerative disease associations under investigation
Epigenetic Regulation
IL32 expression is epigenetically regulated:
- DNA methylation patterns in disease states
- Histone modifications affecting promoter activity
- Non-coding RNA-mediated regulation
Cellular and Molecular Interactions
Neuronal IL-32 Functions
In neurons, IL-32 has distinct effects [8/https://pubmed.ncbi.nlm.nih.gov/22572556/):
Intracellular signaling:
- Can function without secretion
- Direct effects on neuronal survival pathways
- Modulation of synaptic protein expression
- Regulated by neuronal activity
- May influence synaptic plasticity
- Contributes to activity-dependent inflammation
Microglial Interactions
Microglia respond to IL-32 through multiple mechanisms [11/https://pubmed.ncbi.nlm.nih.gov/26284489/):
Activation states:
- Promotes M1-like pro-inflammatory phenotype
- Enhances antigen presentation capacity
- Modulates phagocytic activity
- TREM2 signaling modulates IL-32 responses
- IL-32 may affect TREM2-dependent clearance
- Bidirectional communication influences pathology
Astrocyte Cross-talk
IL-32 affects astrocyte function [14/https://pubmed.ncbi.nlm.nih.gov/25309408/):
Reactive phenotypes:
- Induces A1 neurotoxic reactive astrocytes
- Affects metabolic support functions
- Modulates potassium handling
- Interactions with endothelial cells
- Blood-brain barrier regulation
- Pericyte responses
Neuroimmune Interface
Peripheral-CNS Communication
IL-32 serves as a link between peripheral and CNS immunity:
Systemic inflammation:
- Elevated peripheral IL-32 during infection
- Can cross or affect the blood-brain barrier
- Contributes to sickness behavior
- Monocyte entry to CNS carrying IL-32
- T cell-derived IL-32 in CNS lesions
- NK cell contributions
Cytokine Networks
IL-32 interacts with the broader cytokine network:
Pro-inflammatory amplification:
- Induces TNF-α, IL-1β, IL-6 production
- Creates feed-forward inflammatory loops
- Amplifies existing inflammation
- Can be modulated by IL-10, TGF-β
- Negative feedback mechanisms exist
- Therapeutic implications
Clinical Perspectives
Patient Stratification
IL-32 levels may help stratify patients:
- High IL-32 associated with active inflammation
- Different patterns across disease stages
- Potential for personalized approaches
Monitoring Disease Activity
Serial IL-32 measurement could track:
- Treatment response
- Disease progression
- Relapse risk
Therapeutic Implications
Understanding IL-32 biology informs:
- Target selection for new therapies
- Combination approaches
- Timing of interventions
Environmental and Lifestyle Factors
Diet Effects
Dietary factors influence IL-32:
- High-fat diets increase IL-32 expression
- Anti-inflammatory diets may reduce levels
- Nutritional interventions as modulators
Exercise Effects
Exercise modulates IL-32 [30](https://pubmed.ncbi.nlm.nih.gov/22902874/):
- Acute exercise transiently increases IL-32
- Chronic exercise may reduce baseline levels
- Mechanisms involve muscle-brain crosstalk
Stress Effects
Psychological stress affects IL-32:
- Stress hormones modulate expression
- Chronic stress increases inflammation
- Stress reduction benefits align
Emerging Research Areas
Single-Cell Technologies
Single-cell approaches reveal:
- Cell-type specific IL-32 expression
- Heterogeneity in glial responses
- Novel population definitions
Systems Immunology
Integration approaches provide:
- Network-level understanding
- Predictive modeling
- Personalized medicine foundation
Computational Biology
Bioinformatics applications include:
- Disease subtype classification
- Treatment response prediction
- Biomarker discovery
Conclusion
IL-32 represents a critical nexus between peripheral immunity and neuroinflammation. Its unique structure, multiple receptor interactions, and diverse biological activities make it an important player in neurodegenerative disease pathogenesis. While significant progress has been made in understanding IL-32's basic biology, substantial work remains to translate this knowledge into clinical applications. The development of IL-32-targeted therapies holds promise for neurodegenerative diseases where neuroinflammation plays a central role.
See Also (Updated)
- [Alzheimer's Disease)(/diseases/alzheimer-disease)
- [Parkinson's Disease](/diseases/parkinsons-disease)
- [Multiple Sclerosis](/diseases/multiple-sclerosis)
- [Neuroinflammation](/mechanisms/neuroinflammation-pathway)
- [Cytokine Signaling](/mechanisms/cytokine-signaling-neurodegeneration)
- [Microglia](/cell-types/microglia-neuroinflammation)
- [Astrocytes](/cell-types/astrocytes)
- [TREM2](/proteins/trem2-protein)
- [NF-κB Signaling](/mechanisms/nfkb-signaling-pathway)
- [MAPK Signaling](/mechanisms/mapk-signaling-pathway)
- [Inflammasome](/mechanisms/nlrp3-inflammasome)
See Also
- [Alzheimer's Disease](/diseases/alzheimer-disease)
- [Parkinson's Disease](/diseases/parkinsons-disease)
- [Multiple Sclerosis](/diseases/multiple-sclerosis)
- [Neuroinflammation](/mechanisms/neuroinflammation-pathway)
- [Cytokine Signaling](/mechanisms/cytokine-signaling-neurodegeneration)
- [Microglia](/cell-types/microglia-neuroinflammation)
- [Astrocytes](/cell-types/astrocytes)
External Links
- [IL32 Gene - NCBI](https://www.ncbi.nlm.nih.gov/gene/9235)
- [IL32 Protein - UniProt](https://www.uniprot.org/uniprot/P24001)
- [OMIM: IL32](https://www.omim.org/entry/607528)
- [Ensembl: IL32](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000127124)
References
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| slug | genes-il32 |
| kg_node_id | IL32 |
| entity_type | gene |
| origin_type | v1_polymorphic_backfill |
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| wiki_page_id | wp-034cf43857f7 |
| __merged_from | {'merged_at': '2026-05-13', 'unprefixed_id': 'genes-il32'} |
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