Component

Cytosolic phosphoenolpyruvate carboxykinase / PCK1

Cytosolic gluconeogenic enzyme measured in renal ammoniagenic adaptation.

2 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 acts on it

  1. Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats.

    Potassium → Cytosolic phosphoenolpyruvate carboxykinase / PCK1 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.
    endpoint
    Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats.
    experimental-exposure
    Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
    experimental_model
    Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
    limitations
    Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rattus norvegicus
    plain_language
    The carbon-processing arm of the ammoniagenic/gluconeogenic pathway adapted alongside the nitrogen-releasing enzymes.
    primary_references
    [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
    tissue_or_cell_type
    renal proximal tubule and whole-kidney excretion
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1014–1026

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft

    ### k-deprivation-pck1 Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carbon-processing arm of the ammoniagenic/gluconeogenic pathway adapted alongside the nitrogen-releasing enzymes. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Pyruvate kinase and phosphoenolpyruvate carboxykinase activities in the Echinococcus granulosus cyst wall were markedly inhibited by mebendazole and albendazole while fumarate hydratase activity showed no apparent change, with inhibition rates in the mebendazole group of 85 to 88% and 90 to 92% respectively against 55.3% and 71.6% in the albendazole group, suggesting that these two enzymes may be an important site attacked by effective anti-hydatid drugs.

    Mebendazole → Pyruvate kinase of the Echinococcus cyst wall source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mebendazole-research/8010090.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "581715173f3b7176eda8a357166f1647196f646769b75ee7ca9070342a9c312b", "start_char": 0, "end_char": 933, "text_sha256": "581715173f3b7176eda8a357166f1647196f646769b75ee7ca9070342a9c312b"}
    experimental_model
    Enzyme activity assays on Echinococcus granulosus cyst wall from infected mice after 7 to 14 days of treatment
    exposure
    Mebendazole 25 to 50, albendazole 300 and praziquantel 500 milligrams per kilogram daily by gavage
    limitations
    An in vivo enzyme measurement with a head-to-head dose comparison, though the doses are not equipotent and the cyst wall is one tissue.
    nutrient_topic
    Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole
    organism
    Cestode
    plain_language
    In a live infection mebendazole shut down two sugar-handling enzymes almost completely, and did so harder than albendazole.
    primary_references
    [mbz-p8010090] Effects of mebendazole, albendazole, and praziquantel on fumarate hydratase, pyruvate kinase, and phosphoenolpyruvate carboxykinase of Echinococcus granulosus cyst wall harbored in mice. (1994). https://pubmed.ncbi.nlm.nih.gov/8010090/
    tissue_or_cell_type
    Hydatid cyst wall

    Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 251–262

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme activity assays on Echinococcus granulosus cyst wall from infected mice after 7 to 14 days of treatment · source_derived_draft · unverified_draft

    ### mbz-inhibits-pk-and-pepck Pyruvate kinase and phosphoenolpyruvate carboxykinase activities in the Echinococcus granulosus cyst wall were markedly inhibited by mebendazole and albendazole while fumarate hydratase activity showed no apparent change, with inhibition rates in the mebendazole group of 85 to 88% and 90 to 92% respectively against 55.3% and 71.6% in the albendazole group, suggesting that these two enzymes may be an important site attacked by effective anti-hydatid drugs. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: In a live infection mebendazole shut down two sugar-handling enzymes almost completely, and did so harder than albendazole. organism: Cestode tissue_or_cell_type: Hydatid cyst wall experimental_model: Enzyme activity assays on Echinococcus granulosus cyst wall from infected mice after 7 to 14 days of treatment limitations: An in vivo enzyme measurement with a head-to-head dose comparison, though the doses are not equipotent and the cyst wall is one tissue. exposure: Mebendazole 25 to 50, albendazole 300 and praziquantel 500 milligrams per kilogram daily by gavage evidence_span: {"source_cache": "artifacts/mebendazole-research/8010090.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "581715173f3b7176eda8a357166f1647196f646769b75ee7ca9070342a9c312b", "start_char": 0, "end_char": 933, "text_sha256": "581715173f3b7176eda8a357166f1647196f646769b75ee7ca9070342a9c312b"} [mbz-p8010090] Effects of mebendazole, albendazole, and praziquantel on fumarate hydratase, pyruvate kinase, and phosphoenolpyruvate carboxykinase of Echinococcus granulosus cyst wall harbored in mice. (1994). https://pubmed.ncbi.nlm.nih.gov/8010090/
    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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