Component
Receptor activator of NF-kappa-B / TNFRSF11A / RANK
Independent biological entity. Read linked claims for experimental scope and context.
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
Rank-null mice lacked osteoclasts and developed osteopetrosis; marrow transplantation or receptor re-expression restored osteoclast development.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Rank-null mice and genetic rescue
- limitations
- Complete receptor loss is a machinery defect, not evidence of nutritional calcium deficiency.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Mus musculus
- plain_language
- RANK is necessary for normal formation of bone-resorbing cells in this mouse model.
- primary_references
- [li2000] RANK is the intrinsic hematopoietic cell surface receptor that controls osteoclastogenesis and regulation of bone mass and calcium metabolism (2000). https://pubmed.ncbi.nlm.nih.gov/10677500/ DOI: 10.1073/pnas.97.4.1566
- tissue_or_cell_type
- Bone and hematopoietic precursors
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 1059–1068
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rank-null mice and genetic rescue · source_derived_draft · unverified_draft
### rank-loss-blocks-osteoclast-formation Rank-null mice lacked osteoclasts and developed osteopetrosis; marrow transplantation or receptor re-expression restored osteoclast development. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: RANK is necessary for normal formation of bone-resorbing cells in this mouse model. organism: Mus musculus tissue_or_cell_type: Bone and hematopoietic precursors experimental_model: Rank-null mice and genetic rescue limitations: Complete receptor loss is a machinery defect, not evidence of nutritional calcium deficiency. [li2000] RANK is the intrinsic hematopoietic cell surface receptor that controls osteoclastogenesis and regulation of bone mass and calcium metabolism (2000). https://pubmed.ncbi.nlm.nih.gov/10677500/ DOI: 10.1073/pnas.97.4.1566
Complete structured claim and evidence
What acts on it
Retinoic acid suppressed RANK and RANKL-driven osteoclast differentiation in progenitor cultures.
Experimental context and source evidence
- cross_nutrient
- Retinoid/bone-cell stage-dependent response.
- experimental_model
- Human and mouse osteoclast progenitors.
- limitations
- Does not negate whole-bone resorption results; cell stage and neighboring cells differ.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens; Mus musculus
- plain_language
- The response differs when the experiment starts with isolated precursor cells.
- primary_references
- [va-hu2010] Retinoic acid increases proliferation of human osteoclast progenitors and inhibits RANKL-stimulated osteoclast differentiation by suppressing RANK (2010). https://pubmed.ncbi.nlm.nih.gov/20949013/ DOI: 10.1371/journal.pone.0013305
- tissue_or_cell_type
- Osteoclast precursors
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1638–1648
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and mouse osteoclast progenitors. · source_derived_draft · unverified_draft
### va-retinoic-acid-precursor-rank Retinoic acid suppressed RANK and RANKL-driven osteoclast differentiation in progenitor cultures. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response differs when the experiment starts with isolated precursor cells. organism: Homo sapiens; Mus musculus tissue_or_cell_type: Osteoclast precursors experimental_model: Human and mouse osteoclast progenitors. limitations: Does not negate whole-bone resorption results; cell stage and neighboring cells differ. cross_nutrient: Retinoid/bone-cell stage-dependent response. [va-hu2010] Retinoic acid increases proliferation of human osteoclast progenitors and inhibits RANKL-stimulated osteoclast differentiation by suppressing RANK (2010). https://pubmed.ncbi.nlm.nih.gov/20949013/ DOI: 10.1371/journal.pone.0013305
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.