Component
Oxidative phosphorylation
Oxidative phosphorylation. Species, exposure and limitations are retained in each linked claim.
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.
Where it participates (unsigned role)
GABA transporter GAT2 modulates macrophage function and GAT2 deficiency lowers the production of interleukin-1 beta in proinflammatory macrophages, mechanistically GAT2 deficiency boosts the betaine, S-adenosylmethionine and hypoxanthine metabolic pathway to inhibit transcription factor KID3 expression through increased DNA methylation in its promoter region, KID3 regulates oxidative phosphorylation via targeting the expression of related genes and is also critical for NLRP3-ASC-caspase-1 complex formation, and GAT2 deficiency attenuates macrophage-mediated inflammatory responses in vivo including lipopolysaccharide-induced sepsis, infection-induced pneumonia and high-fat diet-induced obesity.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/gaba-research/33827820.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c654d761170222f117b179e232f555803d6a7cadcfb2eed7b95c45539787cff", "start_char": 0, "end_char": 1140, "text_sha256": "7c654d761170222f117b179e232f555803d6a7cadcfb2eed7b95c45539787cff"}
- experimental_model
- Transporter deficiency with metabolic pathway analysis, promoter methylation and three in vivo inflammatory models
- exposure
- GAT2 deficiency in macrophages, with lipopolysaccharide sepsis, infection-induced pneumonia and high-fat diet models
- limitations
- The mechanism assigned here is metabolic and transcriptional, running through methylation of a transcription factor promoter, rather than an electrophysiological one.
- nutrient_topic
- GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
- organism
- Mouse
- plain_language
- Taking away the carrier that moves GABA into the macrophage lowered its main inflammatory output, through a metabolic route and not an electrical one.
- primary_references
- [gb-p33827820] GABA transporter sustains IL-1β production in macrophages. (2021). https://pubmed.ncbi.nlm.nih.gov/33827820/ DOI: 10.1126/sciadv.abe9274
- tissue_or_cell_type
- Proinflammatory macrophage
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter deficiency with metabolic pathway analysis, promoter methylation and three in vivo inflammatory models · source_derived_draft · unverified_draft
### gb-the-transporter-sustains-il1b GABA transporter GAT2 modulates macrophage function and GAT2 deficiency lowers the production of interleukin-1 beta in proinflammatory macrophages, mechanistically GAT2 deficiency boosts the betaine, S-adenosylmethionine and hypoxanthine metabolic pathway to inhibit transcription factor KID3 expression through increased DNA methylation in its promoter region, KID3 regulates oxidative phosphorylation via targeting the expression of related genes and is also critical for NLRP3-ASC-caspase-1 complex formation, and GAT2 deficiency attenuates macrophage-mediated inflammatory responses in vivo including lipopolysaccharide-induced sepsis, infection-induced pneumonia and high-fat diet-induced obesity. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: Taking away the carrier that moves GABA into the macrophage lowered its main inflammatory output, through a metabolic route and not an electrical one. organism: Mouse tissue_or_cell_type: Proinflammatory macrophage experimental_model: Transporter deficiency with metabolic pathway analysis, promoter methylation and three in vivo inflammatory models limitations: The mechanism assigned here is metabolic and transcriptional, running through methylation of a transcription factor promoter, rather than an electrophysiological one. exposure: GAT2 deficiency in macrophages, with lipopolysaccharide sepsis, infection-induced pneumonia and high-fat diet models evidence_span: {"source_cache": "artifacts/gaba-research/33827820.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c654d761170222f117b179e232f555803d6a7cadcfb2eed7b95c45539787cff", "start_char": 0, "end_char": 1140, "text_sha256": "7c654d761170222f117b179e232f555803d6a7cadcfb2eed7b95c45539787cff"} [gb-p33827820] GABA transporter sustains IL-1β production in macrophages. (2021). https://pubmed.ncbi.nlm.nih.gov/33827820/ DOI: 10.1126/sciadv.abe9274
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
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.