Component
Human HEK293T pyruvate efflux assay
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
HEK293T cells expressing reference SLC16A11 showed approximately 45 percent higher pyruvate efflux rate than empty-vector controls in the reported assay.
Experimental context and source evidence
- experimental_model
- Human HEK293T cells expressing human reference SLC16A11-V5 and pyronic FRET sensor
- exposure
- Addition and withdrawal of 0.4 mM pyruvate; neutral pH; Figure 3E reports n=11 and P<0.05. Methods: 2 microgram pyronic and 2 microgram transporter/empty-vector plasmid, transfected 24 hours after plating on coverslips 72 hours before assay.
- limitations
- Selected primary main-text results, figure legend and methods reviewed through indexed PMC passages; supplements not independently reviewed. Difference was observed at neutral pH, not at acidic pH. This is not a K562 experiment and does not establish the mechanism of the genetic interaction. SLC16A11 has intracellular and cell-surface pools; pyruvate transport direction depends on gradients.
- organism
- Human
- primary_locator
- Results: SLC16A11 is a H+-coupled monocarboxylate transporter; Figure 3D-E; pyruvate transport methods.
- primary_references
- https://doi.org/10.1016/j.cell.2017.06.011
SLC16A11 and mitochondrial glutathione: published screen connection and transport evidence · lines 51–57
Primary sources 2022 and 2017, plus labelled descriptive reanalysis on 2026-09-20. · supports · Human HEK293T cells expressing human reference SLC16A11-V5 and pyronic FRET sensor · source_derived_draft · unverified_draft
HEK293T cells expressing reference SLC16A11 showed approximately 45 percent higher pyruvate efflux rate than empty-vector controls in the reported assay. primary_references: https://doi.org/10.1016/j.cell.2017.06.011 primary_locator: Results: SLC16A11 is a H+-coupled monocarboxylate transporter; Figure 3D-E; pyruvate transport methods. organism: Human experimental_model: Human HEK293T cells expressing human reference SLC16A11-V5 and pyronic FRET sensor exposure: Addition and withdrawal of 0.4 mM pyruvate; neutral pH; Figure 3E reports n=11 and P<0.05. Methods: 2 microgram pyronic and 2 microgram transporter/empty-vector plasmid, transfected 24 hours after plating on coverslips 72 hours before assay. limitations: Selected primary main-text results, figure legend and methods reviewed through indexed PMC passages; supplements not independently reviewed. Difference was observed at neutral pH, not at acidic pH. This is not a K562 experiment and does not establish the mechanism of the genetic interaction. SLC16A11 has intracellular and cell-surface pools; pyruvate transport direction depends on gradients.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
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This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.