Component

Human soluble guanylate cyclase alpha1-beta1 heterodimer

Human soluble guanylate cyclase alpha1-beta1 heterodimer. Species, exposure and limitations are retained in each linked 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. Recombinant human soluble guanylate cyclase converted GTP to cGMP and pyrophosphate; both products inhibited enzyme activity in the kinetic assays.

    Human soluble guanylate cyclase alpha1-beta1 heterodimer → Cyclic guanosine monophosphate source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/citrulline-research/10995472.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c117699ec7c07cc54d779cc0e8274c07555b0ec93498daa8a484652edc219244", "start_char": 0, "end_char": 1300, "text_sha256": "c117699ec7c07cc54d779cc0e8274c07555b0ec93498daa8a484652edc219244"}
    experimental_model
    Recombinant heterodimer purification and enzyme kinetics
    exposure
    NO donor and YC-1 activation; GTP, cGMP and pyrophosphate kinetics
    limitations
    Purified-enzyme study; not a citrulline supplementation trial.
    nutrient_topic
    Citrulline research collection; topical membership is not evidence of a direct dietary effect. · L-Citrulline
    organism
    Human alpha1-beta1 sGC expressed in insect cells
    plain_language
    The NO receptor makes a second messenger, cGMP, linking the initial signal to downstream responses.
    primary_references
    [citrulline-p10995472] Human recombinant soluble guanylyl cyclase: expression, purification, and regulation. (2000). https://pubmed.ncbi.nlm.nih.gov/10995472/ DOI: 10.1073/pnas.190333697
    tissue_or_cell_type
    GTP conversion, heme and product inhibition

    Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 489–500

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant heterodimer purification and enzyme kinetics · source_derived_draft · unverified_draft

    ### citrulline-sgc-cgmp Recombinant human soluble guanylate cyclase converted GTP to cGMP and pyrophosphate; both products inhibited enzyme activity in the kinetic assays. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: The NO receptor makes a second messenger, cGMP, linking the initial signal to downstream responses. organism: Human alpha1-beta1 sGC expressed in insect cells tissue_or_cell_type: GTP conversion, heme and product inhibition experimental_model: Recombinant heterodimer purification and enzyme kinetics limitations: Purified-enzyme study; not a citrulline supplementation trial. exposure: NO donor and YC-1 activation; GTP, cGMP and pyrophosphate kinetics evidence_span: {"source_cache": "artifacts/citrulline-research/10995472.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c117699ec7c07cc54d779cc0e8274c07555b0ec93498daa8a484652edc219244", "start_char": 0, "end_char": 1300, "text_sha256": "c117699ec7c07cc54d779cc0e8274c07555b0ec93498daa8a484652edc219244"} [citrulline-p10995472] Human recombinant soluble guanylyl cyclase: expression, purification, and regulation. (2000). https://pubmed.ncbi.nlm.nih.gov/10995472/ DOI: 10.1073/pnas.190333697
    Complete structured claim and evidence

What acts on it

  1. NO binding to the beta1 H-NOX region drove structural changes that increased human soluble guanylate cyclase activity.

    NO → Human soluble guanylate cyclase alpha1-beta1 heterodimer source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/citrulline-research/31514202.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3001c79d449d8a5545278fdaa6dd7a2dd9e1a67b6e4553d78bbc5848a35362d", "start_char": 0, "end_char": 991, "text_sha256": "e3001c79d449d8a5545278fdaa6dd7a2dd9e1a67b6e4553d78bbc5848a35362d"}
    experimental_model
    Cryo-EM structures in multiple functional states
    exposure
    NO-bound and other functional enzyme states
    limitations
    Structural signal transduction, not a clinical citrulline efficacy experiment.
    nutrient_topic
    Citrulline research collection; topical membership is not evidence of a direct dietary effect. · L-Citrulline
    organism
    Human soluble guanylate cyclase alpha1-beta1
    plain_language
    NO is a signal received by another enzyme, rather than the final vascular response.
    primary_references
    [citrulline-p31514202] Structural insights into the mechanism of human soluble guanylate cyclase. (2019). https://pubmed.ncbi.nlm.nih.gov/31514202/ DOI: 10.1038/s41586-019-1584-6
    tissue_or_cell_type
    NO sensor, transducer and catalytic modules

    Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 684–695

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM structures in multiple functional states · source_derived_draft · unverified_draft

    ### citrulline-no-sgc NO binding to the beta1 H-NOX region drove structural changes that increased human soluble guanylate cyclase activity. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: NO is a signal received by another enzyme, rather than the final vascular response. organism: Human soluble guanylate cyclase alpha1-beta1 tissue_or_cell_type: NO sensor, transducer and catalytic modules experimental_model: Cryo-EM structures in multiple functional states limitations: Structural signal transduction, not a clinical citrulline efficacy experiment. exposure: NO-bound and other functional enzyme states evidence_span: {"source_cache": "artifacts/citrulline-research/31514202.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3001c79d449d8a5545278fdaa6dd7a2dd9e1a67b6e4553d78bbc5848a35362d", "start_char": 0, "end_char": 991, "text_sha256": "e3001c79d449d8a5545278fdaa6dd7a2dd9e1a67b6e4553d78bbc5848a35362d"} [citrulline-p31514202] Structural insights into the mechanism of human soluble guanylate cyclase. (2019). https://pubmed.ncbi.nlm.nih.gov/31514202/ DOI: 10.1038/s41586-019-1584-6
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In cardiac myocytes cyclic GMP is produced by soluble and particulate guanylyl cyclases, the former stimulated by nitric oxide and the latter by natriuretic peptides, and is hydrolyzed to inactive 5-GMP by cyclic GMP phosphodiesterases, cyclic GMP and protein kinase G modulate cardiac contractility, hypertrophy and remodeling and exert cardioprotection, recent studies have revealed that cyclic GMP degradation controlled by phosphodiesterases plays a critical role in the physiological action of cyclic GMP, and several clinical trials are ongoing including a large multicenter trial led by the NIH evaluating sildenafil efficacy in heart failure with preserved ejection fraction.

    Membrane-bound particulate guanylate cyclase and other non-nitric-oxide sources of cyclic GMP → Cyclic guanosine monophosphate source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sildenafil-research/22785374.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14560978d3bfa37c665443c993d21b9c4a0e287c6c8c45672ee35ed55f0c6094", "start_char": 0, "end_char": 1262, "text_sha256": "14560978d3bfa37c665443c993d21b9c4a0e287c6c8c45672ee35ed55f0c6094"}
    experimental_model
    Review of cyclic GMP and protein kinase G signal regulation in the cardiac myocyte
    exposure
    Sources and degradation of cyclic GMP in the myocyte, and phosphodiesterase type 5 inhibition across cardiac pathologies
    limitations
    A review written while the definitive trial was still running, and it names that trial as the test of its own thesis.
    nutrient_topic
    Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. · Sildenafil
    organism
    Animal and human
    plain_language
    The messenger has a second source that answers to natriuretic peptides rather than nitric oxide.
    primary_references
    [sil-p22785374] Cyclic GMP-dependent signaling in cardiac myocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22785374/ DOI: 10.1253/circj.cj-12-0664
    tissue_or_cell_type
    Cardiac myocyte

    Sildenafil: the enzyme it occupies instead of the substrate, why it cannot start a signal it can only preserve, the organic nitrate interaction that follows from that, the homologous retinal enzyme ten-fold away, and the pulmonary circulation where the same mechanism became a second indication (2026-09-22) · lines 613–624

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of cyclic GMP and protein kinase G signal regulation in the cardiac myocyte · source_derived_draft · unverified_draft

    ### sil-two-sources-of-the-messenger In cardiac myocytes cyclic GMP is produced by soluble and particulate guanylyl cyclases, the former stimulated by nitric oxide and the latter by natriuretic peptides, and is hydrolyzed to inactive 5-GMP by cyclic GMP phosphodiesterases, cyclic GMP and protein kinase G modulate cardiac contractility, hypertrophy and remodeling and exert cardioprotection, recent studies have revealed that cyclic GMP degradation controlled by phosphodiesterases plays a critical role in the physiological action of cyclic GMP, and several clinical trials are ongoing including a large multicenter trial led by the NIH evaluating sildenafil efficacy in heart failure with preserved ejection fraction. Condition category: normal nutrient_topic: Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. plain_language: The messenger has a second source that answers to natriuretic peptides rather than nitric oxide. organism: Animal and human tissue_or_cell_type: Cardiac myocyte experimental_model: Review of cyclic GMP and protein kinase G signal regulation in the cardiac myocyte limitations: A review written while the definitive trial was still running, and it names that trial as the test of its own thesis. exposure: Sources and degradation of cyclic GMP in the myocyte, and phosphodiesterase type 5 inhibition across cardiac pathologies evidence_span: {"source_cache": "artifacts/sildenafil-research/22785374.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14560978d3bfa37c665443c993d21b9c4a0e287c6c8c45672ee35ed55f0c6094", "start_char": 0, "end_char": 1262, "text_sha256": "14560978d3bfa37c665443c993d21b9c4a0e287c6c8c45672ee35ed55f0c6094"} [sil-p22785374] Cyclic GMP-dependent signaling in cardiac myocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22785374/ DOI: 10.1253/circj.cj-12-0664
    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.

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