Component
Hoxb1 gene
HOXB1 locus; developmental regulatory studies here use mouse enhancers and embryos.
3 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
Preheadfold RA exposure altered segmental Hoxb1 reporter expression in mouse hindbrain.
Experimental context and source evidence
- evidence_locator
- Abstract
- experimental_model
- RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy.
- exposure
- Experimental excess RA exposure
- limitations
- Timing-specific teratogenic experiment, not ordinary dietary intake.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus
- plain_language
- Excess RA can shift where an embryonic patterning gene is active.
- primary_references
- [va-marshall-1992] Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity (1992). https://www.nature.com/articles/360737a0 DOI: 10.1038/360737a0
- tissue_or_cell_type
- Preheadfold embryos/hindbrain
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1422–1433
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy. · source_derived_draft · unverified_draft
### va-sig-excess-ra-hox-pattern Preheadfold RA exposure altered segmental Hoxb1 reporter expression in mouse hindbrain. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Excess RA can shift where an embryonic patterning gene is active. organism: Mus musculus tissue_or_cell_type: Preheadfold embryos/hindbrain experimental_model: RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy. limitations: Timing-specific teratogenic experiment, not ordinary dietary intake. evidence_locator: Abstract exposure: Experimental excess RA exposure [va-marshall-1992] Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity (1992). https://www.nature.com/articles/360737a0 DOI: 10.1038/360737a0
Complete structured claim and evidence
Where it participates (unsigned role)
The exposed embryos showed rhombomere 2/3 transformation toward 4/5 identity with matching anatomical changes.
Experimental context and source evidence
- evidence_locator
- Abstract
- experimental_model
- RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy.
- exposure
- Experimental excess RA exposure
- limitations
- Not a quantitative human teratogenic threshold.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus
- plain_language
- Excess developmental signaling changed segment identity.
- primary_references
- [va-marshall-1992] Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity (1992). https://www.nature.com/articles/360737a0 DOI: 10.1038/360737a0
- tissue_or_cell_type
- Embryonic hindbrain
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1435–1446
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy. · source_derived_draft · unverified_draft
### va-sig-excess-ra-hindbrain-identity The exposed embryos showed rhombomere 2/3 transformation toward 4/5 identity with matching anatomical changes. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Excess developmental signaling changed segment identity. organism: Mus musculus tissue_or_cell_type: Embryonic hindbrain experimental_model: RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy. limitations: Not a quantitative human teratogenic threshold. evidence_locator: Abstract exposure: Experimental excess RA exposure [va-marshall-1992] Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity (1992). https://www.nature.com/articles/360737a0 DOI: 10.1038/360737a0
Complete structured claim and evidenceA conserved Hoxb1 enhancer containing a RARE mediated RA responsiveness and early neuroectodermal expression.
Experimental context and source evidence
- evidence_locator
- Abstract
- experimental_model
- Mouse Hoxb1 enhancer transgenes; homologous chicken and pufferfish elements.
- exposure
- Enhancer transgenes and RA exposure
- limitations
- Enhancer behavior is not a maternal serum-retinol threshold.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus; comparative chicken/pufferfish enhancer sequences
- plain_language
- Embryonic RA signaling connects to a spatial developmental gene program.
- primary_references
- [va-marshall-1994] A conserved retinoic acid response element required for early expression of the homeobox gene Hoxb-1 (1994). https://www.nature.com/articles/370567a0 DOI: 10.1038/370567a0
- tissue_or_cell_type
- Early embryonic neuroectoderm
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1396–1407
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Hoxb1 enhancer transgenes; homologous chicken and pufferfish elements. · source_derived_draft · unverified_draft
### va-sig-hoxb1-ra-enhancer A conserved Hoxb1 enhancer containing a RARE mediated RA responsiveness and early neuroectodermal expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Embryonic RA signaling connects to a spatial developmental gene program. organism: Mus musculus; comparative chicken/pufferfish enhancer sequences tissue_or_cell_type: Early embryonic neuroectoderm experimental_model: Mouse Hoxb1 enhancer transgenes; homologous chicken and pufferfish elements. limitations: Enhancer behavior is not a maternal serum-retinol threshold. evidence_locator: Abstract exposure: Enhancer transgenes and RA exposure [va-marshall-1994] A conserved retinoic acid response element required for early expression of the homeobox gene Hoxb-1 (1994). https://www.nature.com/articles/370567a0 DOI: 10.1038/370567a0
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.