Component

Human adenosylhomocysteinase / AHCY

Context-specific entity; species, compartment and exposure are stated on each claim.

3 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.

Tracing routes…

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 index AHCY-deficient patient had very low enzyme activity and markedly elevated plasma SAH, SAM and methionine.

    Human adenosylhomocysteinase / AHCY → SAM/SAH accumulation in human AHCY deficiency source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human infant, liver/red-cell/fibroblast assays and genetic analysis.
    limitations
    Single rare-disease case; not evidence of the same block in ordinary dietary variation.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    Abundant methyl-donor substrate can coexist with blocked recycling.
    primary_references
    S-adenosylhomocysteine hydrolase deficiency in a human: a genetic disorder of methionine metabolism. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15024124/ · DOI 10.1073/pnas.0400658101
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 180–186

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human infant, liver/red-cell/fibroblast assays and genetic analysis. · source_derived_draft · unverified_draft

    ## methionine-ahcy-loss Abundant methyl-donor substrate can coexist with blocked recycling. The index AHCY-deficient patient had very low enzyme activity and markedly elevated plasma SAH, SAM and methionine. Model: Human infant, liver/red-cell/fibroblast assays and genetic analysis. Limitations: Single rare-disease case; not evidence of the same block in ordinary dietary variation. Evidence access: Primary abstract S-adenosylhomocysteine hydrolase deficiency in a human: a genetic disorder of methionine metabolism. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15024124/ · DOI 10.1073/pnas.0400658101
    Complete structured claim and evidence

  2. AHCY catalyzes reversible conversion between SAH and adenosine plus homocysteine; product clearance favors net SAH removal.

    Human adenosylhomocysteinase / AHCY → S-Adenosyl-L-homocysteine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Established reaction in the human AHCY-deficiency investigation.
    limitations
    Reaction equilibrium and cellular product removal matter; plasma concentrations do not uniquely define tissue flux.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    After methyl transfer, the spent donor must be processed.
    primary_references
    S-adenosylhomocysteine hydrolase deficiency in a human: a genetic disorder of methionine metabolism. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15024124/ · DOI 10.1073/pnas.0400658101

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 172–178

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Established reaction in the human AHCY-deficiency investigation. · source_derived_draft · unverified_draft

    ## methionine-ahcy-reaction After methyl transfer, the spent donor must be processed. AHCY catalyzes reversible conversion between SAH and adenosine plus homocysteine; product clearance favors net SAH removal. Model: Established reaction in the human AHCY-deficiency investigation. Limitations: Reaction equilibrium and cellular product removal matter; plasma concentrations do not uniquely define tissue flux. Evidence access: Primary abstract S-adenosylhomocysteine hydrolase deficiency in a human: a genetic disorder of methionine metabolism. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15024124/ · DOI 10.1073/pnas.0400658101
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. ADK variants impaired recombinant enzyme activity and were linked to increased adenosine excretion and SAM/SAH/methionine accumulation.

    Human adenosine kinase / ADK → Adenosine removal coupled to the human methionine cycle source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Six affected individuals from three families; exome sequencing and recombinant variant assays.
    limitations
    A functional block of SAH hydrolysis from adenosine accumulation is the mechanistic interpretation; this is not primary AHCY deficiency.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    Removing one reaction product helps keep the recycling pathway moving.
    primary_references
    Adenosine kinase deficiency disrupts the methionine cycle and causes hypermethioninemia, encephalopathy, and abnormal liver function. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21963049/ · DOI 10.1016/j.ajhg.2011.09.004
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 196–202

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Six affected individuals from three families; exome sequencing and recombinant variant assays. · source_derived_draft · unverified_draft

    ## methionine-adk-product-removal Removing one reaction product helps keep the recycling pathway moving. ADK variants impaired recombinant enzyme activity and were linked to increased adenosine excretion and SAM/SAH/methionine accumulation. Model: Six affected individuals from three families; exome sequencing and recombinant variant assays. Limitations: A functional block of SAH hydrolysis from adenosine accumulation is the mechanistic interpretation; this is not primary AHCY deficiency. Evidence access: Primary abstract Adenosine kinase deficiency disrupts the methionine cycle and causes hypermethioninemia, encephalopathy, and abnormal liver function. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21963049/ · DOI 10.1016/j.ajhg.2011.09.004
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards