gene

SOD1

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about SOD1: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.

2867Connections

0Hypotheses

9Analyses

50Outgoing

50Incoming

0Experiments

11Debates

Summary

SOD1 is a gene implicated in neurodegeneration research. Key relationships include: associated with, activates, therapeutic target. Associated with AD, ALS, ALZHEIMER'S DISEASE. Connected to 930 entities in the SciDEX knowledge graph.

View on Wiki →

No AI portrait yet

🧬 Gene Info

Gene Symbol	SOD1
Full Name	Superoxide Dismutase 1
Chromosome	21q22.11
Protein Type	Enzyme
Function	is a copper/zinc-dependent enzyme that catalyzes the dismutation of superoxide radical (O₂⁻) into molecular oxygen (O₂) and hydrogen peroxide (H₂O₂).
Primary Expression	Motor cortex, Spinal cord, Widespread throughout CNS
Subcellular Localization	</strong></td><td>Cytoplasm, Nucleus, Mitochondria (intermembrane space)</td></tr>
Molecular Weight	16 kDa
Amino Acids	154 aa
Pathways	Amyloid, Apoptosis, Autophagy, Epigenetic, Er Stress
Ensembl ID	ENSG00000142168
GeneCards	SOD1
Human Protein Atlas	SOD1
Copper binding site (Cu1)	Catalytic site where superoxide dismutation occurs
Zinc binding sites (Zn1, Zn2)	Structural site that stabilizes the dimer interface
Associated Diseases	AD, Aging, Als, Alzheimer
Known Drugs/Compounds	Amyloid-Beta Oligomers, antisense oligonucleotides, Antisense Oligonucleotides, ARIMOCLOMOL, CISPLATIN, curcumin
Interactions	ACTB, ACTG1, AD, AGING, AKT, AKT1
KG Connections	2201 knowledge graph edges
Databases	GeneCards UniProt NCBI Gene HPA STRING

🧬 3D Structure Comparison — SOD1 Experimental (PDB) vs Predicted (AlphaFold) — click to expand

📄 Experimental Structure

2C9V — X-ray / Cryo-EM

🔮 AI Predicted Structure

P00441 — AlphaFold

Left: Experimental structure from RCSB PDB | Right: AI-predicted structure from AlphaFold | Powered by Mol*

Wiki Pages (12)

Knowledge base pages for this entity

Canonical Page

Pathway Diagram

graph TD
    SOD1["SOD1"] -->|"causes"| ALS["ALS"]
    SOD1["SOD1"] -->|"causes"| FALS["FALS"]
    SOD1["SOD1"] -->|"associated"| AD["AD"]
    SOD1["SOD1"] -->|"associated"| ALS_1["ALS"]
    SOD1["SOD1"] -->|"encodes"| SOD1_protein["SOD1_protein"]
    SOD1["SOD1"] -->|"expressed in"| chromosome_21["chromosome_21"]
    STIP1["STIP1"] -->|"associated"| SOD1["SOD1"]
    LGALS3["LGALS3"] -->|"associated"| SOD1["SOD1"]
    HSPA8["HSPA8"] -->|"associated"| SOD1["SOD1"]
    MCOLN1["MCOLN1"] -->|"associated"| SOD1["SOD1"]
    style SOD1 fill:#4a1a6b,stroke:#4fc3f7,stroke-width:2px,color:#e0e0e0

Outgoing (1390)

Target	Relation	Type	Str
TARDBP	associated_with	gene	1.00
ALS	causes	disease	1.00
FALS	causes	disease	1.00
Amyotrophic Lateral Sclerosis	causes	disease	1.00
AMYOTROPHIC LATERAL SCLEROSIS	causes	gene	1.00
Als	associated_with	disease	1.00
NEURON	associated_with	gene	1.00
DEMENTIA	associated_with	disease	1.00
Amyotrophic Lateral Sclerosis	therapeutic_target	disease	1.00
Als	therapeutic_target	disease	1.00
TNF	associated_with	gene	0.98
Amyotrophic Lateral Sclerosis	activates	disease	0.95
Parkinson	therapeutic_target	disease	0.95
superoxide anion	inhibits	phenotype	0.95
Inflammation	activates	disease	0.95
Lysosome-To-Mitochondria Communication	mediates	pathway	0.95
Amyotrophic Lateral Sclerosis	associated_with	disease	0.95
Familial Amyotrophic Lateral Sclerosis	risk_factor_for	disease	0.95
DNA Oxidative Damage	protects_against	process	0.95
Hypoglossal Nucleus	expressed_in	brain_region	0.92
Familial ALS	risk_factor_for	disease	0.90
Superoxide Radicals	protects_against	compound	0.90
Motor Neurons	expressed_in	cell_type	0.90
Brainstem	expressed_in	brain_region	0.90
Cell Senescence	inhibits	process	0.90
Motor Neuron Degeneration	causes	disease	0.90
protein misfolding	causes	pathway	0.90
Motor Neuron Degeneration	contributes_to	process	0.90
miR-3960	upregulates	biomarker	0.90
oxidative stress	promotes	process	0.90
amyotrophic lateral sclerosis	causes	disease	0.90
FRONTOTEMPORAL DEMENTIA	associated_with	disease	0.90
Gain Of Function Mutations	involved_in	variant	0.90
ALS	associated_with	disease	0.90
ALS	treats	disease	0.90
motor neuron death	contributes_to	process	0.90
AMYOTROPHIC LATERAL SCLEROSIS	therapeutic_target	gene	0.90
AMYOTROPHIC LATERAL SCLEROSIS	activates	gene	0.90
AMYOTROPHIC LATERAL SCLEROSIS	associated_with	gene	0.90
Axonal Degeneration	associated_with	process	0.88
neurodegeneration	associated_with	process	0.88
Neuroinflammation	activates	disease	0.85
Motor Neuron Loss	contributes_to	process	0.85
Alzheimer	therapeutic_target	disease	0.85
Neurodegeneration	therapeutic_target	disease	0.85
Alzheimer's disease	associated_with	disease	0.85
Oxidative Stress	causes	process	0.85
DNA Damage	associated_with	process	0.85
Mitochondrial Damage	causes	process	0.85
Motor Neuron Loss	involved_in	process	0.85

Incoming (1477)

Source	Relation	Type	Str
AMYLOID	associated_with	gene	1.00
ALS	associated_with	gene	1.00
ALZHEIMER'S DISEASE	associated_with	disease	1.00
PARKINSON'S DISEASE	associated_with	gene	1.00
NRF2	associated_with	gene	1.00
HUD	regulates	gene	0.95
HUD	upregulates	protein	0.90
Tofersen	targets	drug	0.90
MTORC1	phosphorylates	protein	0.90
CHK2	phosphorylates	protein	0.90
IL-6	associated_with	gene	0.90
HUD	binds	protein	0.90
Fisetin	upregulates	compound	0.90
Chlorogenic acid	upregulates	compound	0.90
NEUROINFLAMMATION	associated_with	gene	0.90
h-47ab2be5	targets	hypothesis	0.90
h-10b5bf6f	targets	hypothesis	0.90
GENES	associated_with	gene	0.90
ALS	treats	disease	0.90
ATM/Chk2 Pathway	activates	pathway	0.85
ATR/Chk1 Pathway	activates	pathway	0.85
antisense oligonucleotides	inhibits	drug	0.85
CRISPR/Cas9	targets	pathway	0.85
Antisense Oligonucleotides	targets	drug	0.85
RNA interference	inhibits	pathway	0.85
Amyloid-Beta Oligomers	inhibits	compound	0.85
FUS	associated_with	gene	0.82
P2X7 receptor	mediates_release_of	protein	0.80
amyloid-beta oligomers	dysregulates	compound	0.80
PRKCD	activates	gene	0.80
CAMK2D	upregulates	gene	0.80
Lactiplantibacillus plantarum FRT4	activates	drug	0.80
Oligonucleotides	targets	compound	0.80
intermittent hypoxia	inhibits	phenotype	0.80
NFE2L2	associated_with	gene	0.80
ASTROCYTE	activates	gene	0.80
PARKINSON'S DISEASE	therapeutic_target	gene	0.80
C9ORF72	treats	gene	0.80
NEURODEGENERATION	therapeutic_target	gene	0.80
ALS	targets	gene	0.80
116B	upregulates	compound	0.78
FGF21	co_expressed_with	protein	0.75
CASP3	interacts_with	protein	0.75
ALS	activates	disease	0.74
CASP3	associated_with	gene	0.74
NF-KB	associated_with	protein	0.74
AKT	associated_with	gene	0.74
AMPK	associated_with	gene	0.74
AUTOPHAGY	associated_with	gene	0.74
ALS	causes	gene	0.74

Targeting Hypotheses (0)

Hypotheses where this entity is a therapeutic target

Hypothesis	Score	Disease	Analysis
No targeting hypotheses

Mentioning Analyses (9)

Scientific analyses that reference this entity

Experiments (0)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
No experiments found

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
No papers found

Debates (11)

Multi-agent debates referencing this entity

Related Research

Hypotheses and analyses mentioning SOD1 in their description or question text

No additional research found

SOD1

Understanding Entity Pages

Summary

Wiki Pages (12)

SOD1 Protein

SOD1 — Superoxide Dismutase 1

SOD1 Superoxide Dismutase 1 ALS Causal Chain

SOD1 Mutations in Amyotrophic Lateral Sclerosis

SOD1 ALS Pathway

SOD1 (Cu/Zn Superoxide Dismutase)

Pathway Diagram

Outgoing (1390)

Incoming (1477)

Targeting Hypotheses (0)

Mentioning Analyses (9)

How do non-cell autonomous effects of autophagy dysfunction contribute to ALS pa

CRISPR-based therapeutic approaches for neurodegenerative diseases

CRISPR-based therapeutic approaches for neurodegenerative diseases

Epigenetic clocks and biological aging in neurodegeneration

Synaptic pruning by microglia in early AD

TDP-43 phase separation therapeutics for ALS-FTD

Astrocyte reactivity subtypes in neurodegeneration

4R-tau strain-specific spreading patterns in PSP vs CBD

Mechanistic role of APOE in neurodegeneration

Experiments (0)

Related Papers (0)

Debates (11)

PSP and CBD both involve 4R-tau but produce distinct neuropathological patterns

TDP-43 undergoes liquid-liquid phase separation that becomes pathological. Small

TDP-43 phase separation therapeutics for ALS-FTD

PSP and CBD both involve 4R-tau but produce distinct neuropathological patterns

How do non-cell autonomous effects of autophagy dysfunction contribute to ALS pa

Astrocyte reactivity subtypes in neurodegeneration

Analysis question not specified

Synaptic pruning by microglia in early AD

Epigenetic clocks and biological aging in neurodegeneration

Evaluate the potential of CRISPR/Cas9 and related gene editing technologies for

Related Research

SOD1

Understanding Entity Pages

Summary

Wiki Pages (12)

SOD1 Protein

SOD1 — Superoxide Dismutase 1

SOD1 Superoxide Dismutase 1 ALS Causal Chain

SOD1 Mutations in Amyotrophic Lateral Sclerosis

SOD1 ALS Pathway

SOD1 (Cu/Zn Superoxide Dismutase)

SOD1 Mutant Motor Neurons

SOD1-Targeting Therapies for ALS

SOD1 Protein

SOD1 Mutant Motor Neurons

SOD1 (Redirect)

SOD1 Protein (Superoxide Dismutase 1)

Pathway Diagram

Outgoing (1390)

Incoming (1477)

Targeting Hypotheses (0)

Mentioning Analyses (9)

How do non-cell autonomous effects of autophagy dysfunction contribute to ALS pa

CRISPR-based therapeutic approaches for neurodegenerative diseases

CRISPR-based therapeutic approaches for neurodegenerative diseases

Epigenetic clocks and biological aging in neurodegeneration

Synaptic pruning by microglia in early AD

TDP-43 phase separation therapeutics for ALS-FTD

Astrocyte reactivity subtypes in neurodegeneration

4R-tau strain-specific spreading patterns in PSP vs CBD

Mechanistic role of APOE in neurodegeneration

Experiments (0)

Related Papers (0)

Debates (11)

PSP and CBD both involve 4R-tau but produce distinct neuropathological patterns

TDP-43 undergoes liquid-liquid phase separation that becomes pathological. Small

TDP-43 phase separation therapeutics for ALS-FTD

PSP and CBD both involve 4R-tau but produce distinct neuropathological patterns

How do non-cell autonomous effects of autophagy dysfunction contribute to ALS pa

Astrocyte reactivity subtypes in neurodegeneration

Analysis question not specified

Synaptic pruning by microglia in early AD

Epigenetic clocks and biological aging in neurodegeneration

Evaluate the potential of CRISPR/Cas9 and related gene editing technologies for

Related Research