protein

HO-1

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about HO-1: 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.

874Connections
0Hypotheses
0Analyses
50Outgoing
50Incoming
0Experiments
0Debates

Summary

HO-1 is a protein involved in neurodegeneration research. Key relationships include: activates, regulates, associated with. Associated with ALS, Aging, Als. Connected to 523 entities in the SciDEX knowledge graph.

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🔬 Protein Info
Gene SymbolHO
Chromosome5q33.1
Protein FamilyHeme oxygenase family
FunctionHeme Oxygenase-1 (HO-1), also known as heme oxygenase (decycling) 1 (HMOX1), is a 32 kDa inducible enzyme that catalyzes the rate-limiting step in heme degradation
Subcellular LocalizationEndoplasmic reticulum (membrane)
Molecular Weight32,800 Da
Amino Acids288 aa
PathwaysApoptosis, Autophagy, Ferroptosis, Immune Response, Mitochondrial Function
UniProt ID[P09601](https://www.uniprot.org/uniprot/P09601)
GeneCardsHO
Human Protein AtlasHO
Associated Diseasesaging, Als, Cardiomyopathy, disease
InteractionsABCG2, ACHE, AGING, AHR, AKT, ALZHEIMER
KG Connections874 knowledge graph edges
DatabasesGeneCardsNCBI GeneHPASTRING

Wiki Pages (3)

Knowledge base pages for this entity

HO-1 Modulator Therapy

therapy · 1221 words

Heme Oxygenase-1 (HO-1)

protein · 1218 words

Heme Oxygenase-1 (HO-1/HMOX1)

protein · 812 words

Pathway Diagram

graph TD
    HO_1["HO-1"] -->|"Produces"| bilirubin["bilirubin"]
    HO_1["HO-1"] -->|"Inhibits"| inflammation["inflammation"]
    HO_1["HO-1"] -->|"Therapeutic Target"| Fibrosis["Fibrosis"]
    HO_1["HO-1"] -->|"Therapeutic Target"| Carcinoma["Carcinoma"]
    HO_1["HO-1"] -->|"Therapeutic Target"| Als["Als"]
    HO_1["HO-1"] -->|"Therapeutic Target"| Autoimmune["Autoimmune"]
    HO_1["HO-1"] -->|"Therapeutic Target"| Ms["Ms"]
    HO_1["HO-1"] -->|"Inhibits"| Diabetes["Diabetes"]
    NRF2["NRF2"] -->|"Regulates"| HO_1["HO-1"]
    Nrf2["Nrf2"] -->|"Activates"| HO_1["HO-1"]
    ACSL4["ACSL4"] -->|"Therapeutic Target"| HO_1["HO-1"]
    GPX4["GPX4"] -->|"Therapeutic Target"| HO_1["HO-1"]
    SLC7A11["SLC7A11"] -->|"Therapeutic Target"| HO_1["HO-1"]
    style HO_1 fill:#0d47a1,color:#e0e0e0
    style bilirubin fill:#607D8B,color:#e0e0e0
    style inflammation fill:#607D8B,color:#e0e0e0
    style Fibrosis fill:#b71c1c,color:#e0e0e0
    style Carcinoma fill:#b71c1c,color:#e0e0e0
    style Als fill:#b71c1c,color:#e0e0e0
    style Autoimmune fill:#b71c1c,color:#e0e0e0
    style Ms fill:#b71c1c,color:#e0e0e0
    style Diabetes fill:#b71c1c,color:#e0e0e0
    style NRF2 fill:#0d47a1,color:#e0e0e0
    style Nrf2 fill:#0d47a1,color:#e0e0e0
    style ACSL4 fill:#8d4900,color:#e0e0e0
    style GPX4 fill:#8d4900,color:#e0e0e0
    style SLC7A11 fill:#8d4900,color:#e0e0e0

Outgoing (517)

TargetRelationTypeStr
Apoptosisactivatespathway1.00
Inflammationactivatesdisease1.00
Oxidative Stressactivatespathway1.00
NRF2activatesgene1.00
NRF2inhibitsgene1.00

Incoming (357)

SourceRelationTypeStr
OXIDATIVE STRESSactivatesgene1.00
APOPTOSISactivatesgene1.00
NRF2activatesprotein0.90
NRF2regulatesprotein0.90
NEURODEGENERATIONactivatesgene0.90

Targeting Hypotheses (0)

Hypotheses where this entity is a therapeutic target

HypothesisScoreDiseaseAnalysis
No targeting hypotheses

Mentioning Analyses (0)

Scientific analyses that reference this entity

No analyses mention this entity

Experiments (0)

Experimental studies targeting or related to this entity

ExperimentTypeDiseaseScoreFeasibilityModelStatusEst. Cost
No experiments found

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMIDAuthorsJournalYearCitations
No papers found

Debates (0)

Multi-agent debates referencing this entity

No debates reference this entity

Related Research

Hypotheses and analyses mentioning HO-1 in their description or question text

No additional research found