Component
Autophagy activation
Autophagy activation. 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.
What acts on it
Intracellular bacterial infection decreases GABA levels in vitro in macrophages and in vivo in sera, treatment of macrophages with GABA or GABAergic drugs promotes autophagy activation, enhances phagosomal maturation and antimicrobial responses against mycobacterial infection, in macrophages the GABAergic defense is mediated via macrophage type A GABA receptor, intracellular calcium release and the GABA type A receptor-associated protein-like 1, and GABAergic inhibition increases bacterial loads in mice and zebrafish in vivo suggesting that the GABAergic defense plays an essential function in metazoan host defenses.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/gaba-research/30305619.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4d53b15743f61b910fb1db4781905673c81a070c12245068a369548544e3bc6e", "start_char": 0, "end_char": 1146, "text_sha256": "4d53b15743f61b910fb1db4781905673c81a070c12245068a369548544e3bc6e"}
- experimental_model
- Autophagy and phagosome assays in macrophages with receptor and protein dependency, and infection burden in two whole animals
- exposure
- GABA and GABAergic drugs during intracellular mycobacterial infection, with GABAergic inhibition in vivo
- limitations
- The dependency on the receptor and on a specific autophagy protein is tested, and the outcome is measured in two species. The direction is the opposite of the autoimmunity records.
- 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 and zebrafish
- plain_language
- Here the same molecule helps rather than suppresses: it drives the cell to digest the bacteria inside it, and blocking it lets the infection grow.
- primary_references
- [gb-p30305619] GABAergic signaling linked to autophagy enhances host protection against intracellular bacterial infections. (2018). https://pubmed.ncbi.nlm.nih.gov/30305619/ DOI: 10.1038/s41467-018-06487-5
- tissue_or_cell_type
- Macrophage
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Autophagy and phagosome assays in macrophages with receptor and protein dependency, and infection burden in two whole animals · source_derived_draft · unverified_draft
### gb-gaba-helps-the-host-kill-bacteria Intracellular bacterial infection decreases GABA levels in vitro in macrophages and in vivo in sera, treatment of macrophages with GABA or GABAergic drugs promotes autophagy activation, enhances phagosomal maturation and antimicrobial responses against mycobacterial infection, in macrophages the GABAergic defense is mediated via macrophage type A GABA receptor, intracellular calcium release and the GABA type A receptor-associated protein-like 1, and GABAergic inhibition increases bacterial loads in mice and zebrafish in vivo suggesting that the GABAergic defense plays an essential function in metazoan host defenses. 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: Here the same molecule helps rather than suppresses: it drives the cell to digest the bacteria inside it, and blocking it lets the infection grow. organism: Mouse and zebrafish tissue_or_cell_type: Macrophage experimental_model: Autophagy and phagosome assays in macrophages with receptor and protein dependency, and infection burden in two whole animals limitations: The dependency on the receptor and on a specific autophagy protein is tested, and the outcome is measured in two species. The direction is the opposite of the autoimmunity records. exposure: GABA and GABAergic drugs during intracellular mycobacterial infection, with GABAergic inhibition in vivo evidence_span: {"source_cache": "artifacts/gaba-research/30305619.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4d53b15743f61b910fb1db4781905673c81a070c12245068a369548544e3bc6e", "start_char": 0, "end_char": 1146, "text_sha256": "4d53b15743f61b910fb1db4781905673c81a070c12245068a369548544e3bc6e"} [gb-p30305619] GABAergic signaling linked to autophagy enhances host protection against intracellular bacterial infections. (2018). https://pubmed.ncbi.nlm.nih.gov/30305619/ DOI: 10.1038/s41467-018-06487-5
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.