Component
Mitochondrial integrity in Hsd17b10-deficient mouse cells
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
Loss and rescue experiments in conditional mouse-derived cells showed an HSD10 property independent of dehydrogenase activity was required for mitochondrial integrity and cell survival.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse-derived cells and separate Xenopus embryo experiments; human clinical activity comparisons.
- limitations
- Does not justify treating the entire HSD10 disorder by restricting isoleucine.
- nutrient_topic
- L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
- plain_language
- A protein can be essential even when its named metabolic reaction is not the relevant failure.
- primary_references
- A non-enzymatic function of 17beta-hydroxysteroid dehydrogenase type 10 is required for mitochondrial integrity and cell survival. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20077426/ · DOI 10.1002/emmm.200900055
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 218–224
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse-derived cells and separate Xenopus embryo experiments; human clinical activity comparisons. · source_derived_draft · unverified_draft
## isoleucine-hsd10-noncatabolic A protein can be essential even when its named metabolic reaction is not the relevant failure. Loss and rescue experiments in conditional mouse-derived cells showed an HSD10 property independent of dehydrogenase activity was required for mitochondrial integrity and cell survival. Model: Mouse-derived cells and separate Xenopus embryo experiments; human clinical activity comparisons. Limitations: Does not justify treating the entire HSD10 disorder by restricting isoleucine. Evidence access: Primary abstract A non-enzymatic function of 17beta-hydroxysteroid dehydrogenase type 10 is required for mitochondrial integrity and cell survival. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20077426/ · DOI 10.1002/emmm.200900055
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.