Component
Mouse hepatocyte-specific Slc30a10 knockout genotype
Mouse hepatocyte-specific Slc30a10 knockout genotype
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 it acts on
Hepatic Slc30a10 deficiency impaired biliary manganese excretion in mice despite only minimal manganese excess.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- experimental_model
- Whole-body and tissue-specific Slc30a10 knockout mice
- exposure
- Liver-specific Slc30a10 deficiency versus controls.
- limitations
- Minimal systemic excess does not negate the measured biliary transport defect.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Mus musculus
- plain_language
- The liver exporter supplied biliary clearance, while other routes limited whole-body accumulation.
- primary_references
- [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
- tissue_or_cell_type
- Liver canalicular membrane and bile
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 253–264
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and tissue-specific Slc30a10 knockout mice · source_derived_draft · unverified_draft
### mn-trans-slc30a10-hepatic-excretion Hepatic Slc30a10 deficiency impaired biliary manganese excretion in mice despite only minimal manganese excess. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: The liver exporter supplied biliary clearance, while other routes limited whole-body accumulation. organism: Mus musculus tissue_or_cell_type: Liver canalicular membrane and bile experimental_model: Whole-body and tissue-specific Slc30a10 knockout mice limitations: Minimal systemic excess does not negate the measured biliary transport defect. exposure: Liver-specific Slc30a10 deficiency versus controls. cross_nutrient: false [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
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.