Component
Myeloproliferation in mice
Splenomegaly, monocytosis and extramedullary haematopoiesis developing in vivo.
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
Conditional Tet2 loss produced progressive enlargement of the haematopoietic stem-cell compartment and eventual myeloproliferation in vivo, including splenomegaly, monocytosis and extramedullary haematopoiesis.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- duration
- Progressive, in vivo
- experimental_model
- Conditional Tet2-knockout mice followed in vivo
- exposure
- Conditional genetic deletion of Tet2
- limitations
- Myeloproliferation in a conditional knockout mouse is not the same entity as a human myelodysplastic syndrome, and this model deletes the gene rather than reproducing a point mutation.
- organism
- Mus musculus
- plain_language
- Mice without Tet2 went on to develop a blood disorder of overgrowth.
- primary_references
- [moran-crusio-2011] Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation (2011). https://pubmed.ncbi.nlm.nih.gov/21723200/ DOI: 10.1016/j.ccr.2011.06.001
- tissue
- Bone marrow, spleen and peripheral blood
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
TET2 loss and malignancy: the step between a nutrient-responsive enzyme and the disease (2026-09-23) · lines 63–71
Original AI-assisted curation of twelve primary studies located by Europe PMC title search, with every statement drafted from the retrieved abstract. Two pairs share a laboratory and are recorded as one line of evidence each. Genetic loss of function, pharmacological exposure and dietary depletion are kept as separate record types. Not publisher full text. · supports · Conditional Tet2-knockout mice followed in vivo · source_derived_draft · unverified_draft
## tet2-loss-causes-myeloproliferation Conditional Tet2 loss produced progressive enlargement of the haematopoietic stem-cell compartment and eventual myeloproliferation in vivo, including splenomegaly, monocytosis and extramedullary haematopoiesis. Model/species: Conditional Tet2-knockout mice followed in vivo Organism: Mus musculus Tissue/system: Bone marrow, spleen and peripheral blood Exposure: Conditional genetic deletion of Tet2 Duration: Progressive, in vivo Limits: Myeloproliferation in a conditional knockout mouse is not the same entity as a human myelodysplastic syndrome, and this model deletes the gene rather than reproducing a point mutation. Primary reference: [moran-crusio-2011] Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation (2011). https://pubmed.ncbi.nlm.nih.gov/21723200/ DOI: 10.1016/j.ccr.2011.06.001
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.