Component
Histidine uptake into mouse brain slices
Context-specific entity; species, compartment and exposure are stated on each 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
Deleting Pht1 reduced histidine uptake in mouse brain slices by about half; Pept2 expression increased approximately twofold.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Pht1-null and matched wild-type adult mice; brain slices and transporter expression.
- limitations
- Genetic deletion is not dietary histidine deficiency.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- Loss of one transporter altered uptake even with a compensatory response.
- primary_references
- A novel role for PHT1 in the disposition of l-histidine in brain: In vitro slice and in vivo pharmacokinetic studies in wildtype and Pht1 null mice. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27845049/ · DOI 10.1016/j.bcp.2016.11.012
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 90–96
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pht1-null and matched wild-type adult mice; brain slices and transporter expression. · source_derived_draft · unverified_draft
## histidine-pht1-brain-uptake Loss of one transporter altered uptake even with a compensatory response. Deleting Pht1 reduced histidine uptake in mouse brain slices by about half; Pept2 expression increased approximately twofold. Model: Pht1-null and matched wild-type adult mice; brain slices and transporter expression. Limitations: Genetic deletion is not dietary histidine deficiency. Evidence access: Primary full text A novel role for PHT1 in the disposition of l-histidine in brain: In vitro slice and in vivo pharmacokinetic studies in wildtype and Pht1 null mice. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27845049/ · DOI 10.1016/j.bcp.2016.11.012
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.