Component
Mouse liver-specific Slc39a8 knockout genotype
Mouse liver-specific Slc39a8 knockout genotype
2 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
ZIP8-LSKO mice had increased bile manganese; ZIP8 localized to hepatocyte canalicular membranes, supporting biliary manganese reclamation.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- experimental_model
- Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression
- exposure
- Liver-specific Slc39a8 knockout versus controls.
- limitations
- Bile concentration and anatomical localization support reclamation; concentration is not itself a secretion-rate measurement.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Mus musculus
- plain_language
- Liver ZIP8 helps recover manganese from bile.
- primary_references
- [mn-trans-28481222] Hepatic metal ion transporter ZIP8 regulates manganese homeostasis and manganese-dependent enzyme activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28481222/ DOI: 10.1172/jci90896
- tissue_or_cell_type
- Liver, bile and measured extrahepatic tissues
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 162–173
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression · source_derived_draft · unverified_draft
### mn-trans-hepatic-zip8-loss-bile-mn ZIP8-LSKO mice had increased bile manganese; ZIP8 localized to hepatocyte canalicular membranes, supporting biliary manganese reclamation. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Liver ZIP8 helps recover manganese from bile. organism: Mus musculus tissue_or_cell_type: Liver, bile and measured extrahepatic tissues experimental_model: Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression limitations: Bile concentration and anatomical localization support reclamation; concentration is not itself a secretion-rate measurement. exposure: Liver-specific Slc39a8 knockout versus controls. cross_nutrient: false [mn-trans-28481222] Hepatic metal ion transporter ZIP8 regulates manganese homeostasis and manganese-dependent enzyme activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28481222/ DOI: 10.1172/jci90896
Complete structured claim and evidenceLiver-specific Slc39a8 knockout lowered manganese in multiple organs and whole blood in mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- experimental_model
- Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression
- exposure
- Liver-specific Slc39a8 knockout versus controls.
- limitations
- This is a genetic conservation defect; the abstract does not supply dietary depletion thresholds.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Mus musculus
- plain_language
- Loss of liver ZIP8 depleted manganese beyond the liver.
- primary_references
- [mn-trans-28481222] Hepatic metal ion transporter ZIP8 regulates manganese homeostasis and manganese-dependent enzyme activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28481222/ DOI: 10.1172/jci90896
- tissue_or_cell_type
- Liver, bile and measured extrahepatic tissues
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 136–147
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression · source_derived_draft · unverified_draft
### mn-trans-hepatic-zip8-loss-tissue-mn Liver-specific Slc39a8 knockout lowered manganese in multiple organs and whole blood in mice. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of liver ZIP8 depleted manganese beyond the liver. organism: Mus musculus tissue_or_cell_type: Liver, bile and measured extrahepatic tissues experimental_model: Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression limitations: This is a genetic conservation defect; the abstract does not supply dietary depletion thresholds. exposure: Liver-specific Slc39a8 knockout versus controls. cross_nutrient: false [mn-trans-28481222] Hepatic metal ion transporter ZIP8 regulates manganese homeostasis and manganese-dependent enzyme activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28481222/ DOI: 10.1172/jci90896
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.