Component
Cobalamin release from lysosomal lumen to cytosol
Cobalamin release from lysosomal lumen to cytosol
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
The human disorder assigned to pathogenic ABCD4 mutations showed failure of lysosomal vitamin B12 release, resembling the cblF cellular defect.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Abstract
- experimental_model
- Human cblJ disease and cellular characterization
- exposure
- Inherited ABCD4 mutations
- limitations
- Primary abstract supports the release defect; mutation-specific magnitudes were not extracted.
- nutrient_topic
- Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
- organism
- Homo sapiens
- plain_language
- An inherited transporter defect can trap B12 in lysosomes.
- primary_references
- [coelho-2012-abcd4] Mutations in ABCD4 cause a new inborn error of vitamin B12 metabolism (2012). https://pubmed.ncbi.nlm.nih.gov/22922874/ DOI: 10.1038/ng.2386
- tissue_or_cell_type
- Patient-derived cultured cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 557–569
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cblJ disease and cellular characterization · source_derived_draft · unverified_draft
### b12-abcd4-defect-export The human disorder assigned to pathogenic ABCD4 mutations showed failure of lysosomal vitamin B12 release, resembling the cblF cellular defect. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inherited transporter defect can trap B12 in lysosomes. organism: Homo sapiens tissue_or_cell_type: Patient-derived cultured cells experimental_model: Human cblJ disease and cellular characterization limitations: Primary abstract supports the release defect; mutation-specific magnitudes were not extracted. exposure: Inherited ABCD4 mutations cross_nutrient: false evidence_location: Abstract [coelho-2012-abcd4] Mutations in ABCD4 cause a new inborn error of vitamin B12 metabolism (2012). https://pubmed.ncbi.nlm.nih.gov/22922874/ DOI: 10.1038/ng.2386
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.