Component

Rho membrane translocation and GTP binding

Membrane localisation and nucleotide binding of Rho measured together.

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

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. Mevastatin inhibited Rho membrane translocation by about 60 percent and Rho GTP-binding activity by about 78 percent, both reversed by geranylgeranyl diphosphate but not by farnesyl diphosphate.

    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Human endothelial cells
    exposure
    Mevastatin with or without geranylgeranyl diphosphate or farnesyl diphosphate
    limitations
    Measured for Rho as a group by immunoblot and GTP-gamma-S binding, not resolved to individual Rho family members.
    organism
    Human endothelial cells
    plain_language
    Mevastatin inhibited Rho membrane translocation by about 60 percent and Rho GTP-binding activity by about 78 percent, both reversed by geranylgeranyl diphosphate but not by farnesyl diphosphate.
    primary_references
    Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. (1998). https://pubmed.ncbi.nlm.nih.gov/9727051/ DOI: 10.1074/jbc.273.37.24266
    route
    In vitro
    tissue
    Rho GTPase membrane localisation and nucleotide binding

    Atorvastatin: mechanism of action from target occupancy to isoprenoids, transport, muscle and metabolism (2026-09-22) · lines 78–87

    Original AI-assisted curation of twelve primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Findings obtained with mevastatin, simvastatin or the statin class are recorded against those subjects. Study-specific citations, doses, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## statin-inhibits-rho-membrane-translocation Mevastatin inhibited Rho membrane translocation by about 60 percent and Rho GTP-binding activity by about 78 percent, both reversed by geranylgeranyl diphosphate but not by farnesyl diphosphate. Model/species: Human endothelial cells Tissue/system: Rho GTPase membrane localisation and nucleotide binding Exposure: Mevastatin with or without geranylgeranyl diphosphate or farnesyl diphosphate Route: In vitro Duration: Not stated here Limits: Measured for Rho as a group by immunoblot and GTP-gamma-S binding, not resolved to individual Rho family members. Primary reference: Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. (1998). https://pubmed.ncbi.nlm.nih.gov/9727051/ DOI: 10.1074/jbc.273.37.24266 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    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