Component
Mouse haematopoietic stem and progenitor cell self-renewal
Self-renewal measured by competitive transplantation and serial replating.
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 acts on it
Conditional deletion of Tet2 in the mouse haematopoietic compartment increased stem-cell self-renewal in competitive transplant assays, and Tet2 heterozygous mice also showed increased self-renewal and extramedullary haematopoiesis.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- duration
- In vivo, to the development of disease
- experimental_model
- Conditional Tet2-knockout mice; competitive transplantation
- exposure
- Conditional genetic deletion of Tet2; homozygous and heterozygous
- limitations
- Haploinsufficiency means one damaged copy already changes the phenotype; this is a genetic model, not a nutritional one.
- organism
- Mus musculus
- plain_language
- Losing Tet2 made blood stem cells renew themselves more than they should.
- 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
- Haematopoietic stem cell compartment
- 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 53–61
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; competitive transplantation · source_derived_draft · unverified_draft
## tet2-loss-increases-hspc-self-renewal Conditional deletion of Tet2 in the mouse haematopoietic compartment increased stem-cell self-renewal in competitive transplant assays, and Tet2 heterozygous mice also showed increased self-renewal and extramedullary haematopoiesis. Model/species: Conditional Tet2-knockout mice; competitive transplantation Organism: Mus musculus Tissue/system: Haematopoietic stem cell compartment Exposure: Conditional genetic deletion of Tet2; homozygous and heterozygous Duration: In vivo, to the development of disease Limits: Haploinsufficiency means one damaged copy already changes the phenotype; this is a genetic model, not a nutritional one. 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 evidenceRestoring endogenous Tet2 expression in a reversible transgenic RNAi mouse reversed aberrant haematopoietic stem and progenitor cell self-renewal both in vitro and in vivo.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- duration
- In vitro and in vivo after restoration
- experimental_model
- Reversible transgenic RNAi mouse permitting Tet2 knockdown and restoration
- exposure
- Genetic restoration of endogenous Tet2 expression after knockdown
- limitations
- Restoring a knockdown is not the same as correcting a mutated allele in a patient, and the reversal was measured as self-renewal rather than as cure of an established leukaemia.
- organism
- Mus musculus
- plain_language
- Switching Tet2 back on undid the abnormal renewal, which is the strongest sign the enzyme itself was responsible.
- primary_references
- [cimmino-2017] Restoration of TET2 function blocks aberrant self-renewal and leukemia progression (2017). https://pubmed.ncbi.nlm.nih.gov/28823558/ DOI: 10.1016/j.cell.2017.07.032
- tissue
- Haematopoietic stem and progenitor cells
- 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 93–101
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 · Reversible transgenic RNAi mouse permitting Tet2 knockdown and restoration · source_derived_draft · unverified_draft
## tet2-restoration-reverses-self-renewal Restoring endogenous Tet2 expression in a reversible transgenic RNAi mouse reversed aberrant haematopoietic stem and progenitor cell self-renewal both in vitro and in vivo. Model/species: Reversible transgenic RNAi mouse permitting Tet2 knockdown and restoration Organism: Mus musculus Tissue/system: Haematopoietic stem and progenitor cells Exposure: Genetic restoration of endogenous Tet2 expression after knockdown Duration: In vitro and in vivo after restoration Limits: Restoring a knockdown is not the same as correcting a mutated allele in a patient, and the reversal was measured as self-renewal rather than as cure of an established leukaemia. Primary reference: [cimmino-2017] Restoration of TET2 function blocks aberrant self-renewal and leukemia progression (2017). https://pubmed.ncbi.nlm.nih.gov/28823558/ DOI: 10.1016/j.cell.2017.07.032
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.