Component

The inactive ALDH2*2 subunit carrying lysine for glutamate at position 487

The inactive ALDH2*2 subunit carrying lysine for glutamate at position 487. Species, exposure and limitations are retained in each linked claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

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What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. The inactive ALDH2 subunit carries a substitution of lysine for glutamate at position 487, and correlating genotype with phenotype in 24 Japanese livers shows the allele encoding the abnormal subunit is dominant.

    The inactive ALDH2*2 subunit carrying lysine for glutamate at position 487 → Human mitochondrial aldehyde dehydrogenase 2 / ALDH2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/2562960.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f0722fad2747c7b723bce352582f07519b1b9b964edadb8674740458475efe1", "start_char": 0, "end_char": 800, "text_sha256": "0f0722fad2747c7b723bce352582f07519b1b9b964edadb8674740458475efe1"}
    experimental_model
    Polymerase chain reaction genotyping of 24 Japanese livers against enzyme phenotype
    exposure
    ALDH2 genotype compared with measured enzyme activity
    limitations
    Establishes dominance of the inactive allele, so heterozygotes are affected. The sample is 24 livers.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Human
    plain_language
    One bad copy is enough, because the faulty subunit poisons the four-part enzyme.
    primary_references
    [alcohol-p2562960] Genotypes for aldehyde dehydrogenase deficiency and alcohol sensitivity. The inactive ALDH2(2) allele is dominant. (1989). https://pubmed.ncbi.nlm.nih.gov/2562960/ DOI: 10.1172/jci113875
    tissue_or_cell_type
    Liver
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 150–161

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polymerase chain reaction genotyping of 24 Japanese livers against enzyme phenotype · source_derived_draft · unverified_draft

    ### alcohol-aldh2-allele-dominant The inactive ALDH2 subunit carries a substitution of lysine for glutamate at position 487, and correlating genotype with phenotype in 24 Japanese livers shows the allele encoding the abnormal subunit is dominant. Condition category: machinery_impairment nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: One bad copy is enough, because the faulty subunit poisons the four-part enzyme. organism: Human tissue_or_cell_type: Liver experimental_model: Polymerase chain reaction genotyping of 24 Japanese livers against enzyme phenotype limitations: Establishes dominance of the inactive allele, so heterozygotes are affected. The sample is 24 livers. exposure: ALDH2 genotype compared with measured enzyme activity evidence_span: {"source_cache": "artifacts/alcohol-research/2562960.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f0722fad2747c7b723bce352582f07519b1b9b964edadb8674740458475efe1", "start_char": 0, "end_char": 800, "text_sha256": "0f0722fad2747c7b723bce352582f07519b1b9b964edadb8674740458475efe1"} [alcohol-p2562960] Genotypes for aldehyde dehydrogenase deficiency and alcohol sensitivity. The inactive ALDH2(2) allele is dominant. (1989). https://pubmed.ncbi.nlm.nih.gov/2562960/ DOI: 10.1172/jci113875
    Complete structured claim and evidence

  2. ALDH2 deficiency promoted alcohol-associated liver cancer by activating oncogenic pathways via oxidised-DNA-enriched extracellular vesicles.

    The inactive ALDH2*2 subunit carrying lysine for glutamate at position 487 → Alcohol-associated liver cancer source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/31279903.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3a0e9d2f127fd9454b41431aa6ed4bdcfd30723cc3acee2a1678015ac5299887", "start_char": 0, "end_char": 2706, "text_sha256": "3a0e9d2f127fd9454b41431aa6ed4bdcfd30723cc3acee2a1678015ac5299887"}
    experimental_model
    ALDH2-deficient mice and human samples with extracellular vesicle analysis
    exposure
    Alcohol exposure on an ALDH2-deficient background
    limitations
    Proposes a specific transmissible mechanism. The oncogenic pathway activation is measured in a model, not in treated patients.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Mouse and human samples
    plain_language
    Damaged DNA is packaged into vesicles that carry the cancer signal to other cells.
    primary_references
    [alcohol-p31279903] ALDH2 deficiency promotes alcohol-associated liver cancer by activating oncogenic pathways via oxidized DNA-enriched extracellular vesicles. (2019). https://pubmed.ncbi.nlm.nih.gov/31279903/ DOI: 10.1016/j.jhep.2019.06.018
    tissue_or_cell_type
    Liver
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 553–564

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ALDH2-deficient mice and human samples with extracellular vesicle analysis · source_derived_draft · unverified_draft

    ### alcohol-aldh2-liver-cancer ALDH2 deficiency promoted alcohol-associated liver cancer by activating oncogenic pathways via oxidised-DNA-enriched extracellular vesicles. Condition category: machinery_impairment nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Damaged DNA is packaged into vesicles that carry the cancer signal to other cells. organism: Mouse and human samples tissue_or_cell_type: Liver experimental_model: ALDH2-deficient mice and human samples with extracellular vesicle analysis limitations: Proposes a specific transmissible mechanism. The oncogenic pathway activation is measured in a model, not in treated patients. exposure: Alcohol exposure on an ALDH2-deficient background evidence_span: {"source_cache": "artifacts/alcohol-research/31279903.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3a0e9d2f127fd9454b41431aa6ed4bdcfd30723cc3acee2a1678015ac5299887", "start_char": 0, "end_char": 2706, "text_sha256": "3a0e9d2f127fd9454b41431aa6ed4bdcfd30723cc3acee2a1678015ac5299887"} [alcohol-p31279903] ALDH2 deficiency promotes alcohol-associated liver cancer by activating oncogenic pathways via oxidized DNA-enriched extracellular vesicles. (2019). https://pubmed.ncbi.nlm.nih.gov/31279903/ DOI: 10.1016/j.jhep.2019.06.018
    Complete structured claim and evidence

  3. ALDH2*2 but not ADH1B*2 is the causative variant allele for Asian alcohol flushing after a low-dose challenge, on correlated pharmacokinetic and pharmacodynamic findings.

    The inactive ALDH2*2 subunit carrying lysine for glutamate at position 487 → The alcohol flush reaction source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/25365528.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa331e891fe46dedf3789025686318b37eae41389f093bda084e4a6d482218", "start_char": 0, "end_char": 1803, "text_sha256": "74fa331e891fe46dedf3789025686318b37eae41389f093bda084e4a6d482218"}
    experimental_model
    Low-dose alcohol challenge in genotyped subjects with paired pharmacokinetics and pharmacodynamics
    exposure
    Low-dose alcohol challenge across ADH1B and ALDH2 genotypes
    limitations
    Separates the two candidate variants by measuring both blood levels and symptoms. A low-dose challenge may not represent ordinary drinking.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Human
    plain_language
    Of the two variants people blame for flushing, only one actually causes it.
    primary_references
    [alcohol-p25365528] ALDH2*2 but not ADH1B*2 is a causative variant gene allele for Asian alcohol flushing after a low-dose challenge: correlation of the pharmacokinetic and pharmacodynamic findings. (2014). https://pubmed.ncbi.nlm.nih.gov/25365528/ DOI: 10.1097/fpc.0000000000000096
    tissue_or_cell_type
    Whole body
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 176–187

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Low-dose alcohol challenge in genotyped subjects with paired pharmacokinetics and pharmacodynamics · source_derived_draft · unverified_draft

    ### alcohol-aldh2-not-adh1b-flush ALDH2*2 but not ADH1B*2 is the causative variant allele for Asian alcohol flushing after a low-dose challenge, on correlated pharmacokinetic and pharmacodynamic findings. Condition category: machinery_impairment nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Of the two variants people blame for flushing, only one actually causes it. organism: Human tissue_or_cell_type: Whole body experimental_model: Low-dose alcohol challenge in genotyped subjects with paired pharmacokinetics and pharmacodynamics limitations: Separates the two candidate variants by measuring both blood levels and symptoms. A low-dose challenge may not represent ordinary drinking. exposure: Low-dose alcohol challenge across ADH1B and ALDH2 genotypes evidence_span: {"source_cache": "artifacts/alcohol-research/25365528.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa331e891fe46dedf3789025686318b37eae41389f093bda084e4a6d482218", "start_char": 0, "end_char": 1803, "text_sha256": "74fa331e891fe46dedf3789025686318b37eae41389f093bda084e4a6d482218"} [alcohol-p25365528] ALDH2*2 but not ADH1B*2 is a causative variant gene allele for Asian alcohol flushing after a low-dose challenge: correlation of the pharmacokinetic and pharmacodynamic findings. (2014). https://pubmed.ncbi.nlm.nih.gov/25365528/ DOI: 10.1097/fpc.0000000000000096
    Complete structured claim and evidence

  4. Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhanced oesophageal cancer risk.

    The inactive ALDH2*2 subunit carrying lysine for glutamate at position 487 → Oesophageal squamous cell cancer risk source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/19698717.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4262a0549d8e78b4e7719f62bfa61849f3cf6eb3403bf45fe28d32b7d7662c58", "start_char": 0, "end_char": 1706, "text_sha256": "4262a0549d8e78b4e7719f62bfa61849f3cf6eb3403bf45fe28d32b7d7662c58"}
    experimental_model
    Case-control study of oesophageal cancer with ADH1B and ALDH2 genotypes and smoking
    exposure
    Alcohol consumption and smoking across functional genotypes
    limitations
    A gene-environment interaction study. Synergy is reported on a statistical interaction scale, and the design is case-control.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Human
    plain_language
    The variant that makes drinking unpleasant also makes each drink more carcinogenic.
    primary_references
    [alcohol-p19698717] Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhance esophageal cancer risk. (2009). https://pubmed.ncbi.nlm.nih.gov/19698717/ DOI: 10.1053/j.gastro.2009.07.070
    tissue_or_cell_type
    Oesophagus
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 540–551

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case-control study of oesophageal cancer with ADH1B and ALDH2 genotypes and smoking · source_derived_draft · unverified_draft

    ### alcohol-genotype-cancer-synergy Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhanced oesophageal cancer risk. Condition category: machinery_impairment nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The variant that makes drinking unpleasant also makes each drink more carcinogenic. organism: Human tissue_or_cell_type: Oesophagus experimental_model: Case-control study of oesophageal cancer with ADH1B and ALDH2 genotypes and smoking limitations: A gene-environment interaction study. Synergy is reported on a statistical interaction scale, and the design is case-control. exposure: Alcohol consumption and smoking across functional genotypes evidence_span: {"source_cache": "artifacts/alcohol-research/19698717.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4262a0549d8e78b4e7719f62bfa61849f3cf6eb3403bf45fe28d32b7d7662c58", "start_char": 0, "end_char": 1706, "text_sha256": "4262a0549d8e78b4e7719f62bfa61849f3cf6eb3403bf45fe28d32b7d7662c58"} [alcohol-p19698717] Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhance esophageal cancer risk. (2009). https://pubmed.ncbi.nlm.nih.gov/19698717/ DOI: 10.1053/j.gastro.2009.07.070
    Complete structured claim and evidence

In the sources

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