Component
Human SARM1
Human sterile alpha and TIR motif-containing protein 1.
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.
Where it participates (unsigned role)
After axotomy of Sarm1-null mouse DRG neurons, re-expression of active human SARM1 restored rapid axonal NAD+ depletion, whereas E642A did not.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_span
- {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 29", "start_char": 20432, "end_char": 22775, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "e75c162a4b5f51b7e6ef5e20612ed8ebfbe035a41abf81284cb055dfcf860333"}
- experimental_model
- Reconstitution of Sarm1-null E13.5 mouse DRG neurons with SARM1 constructs
- exposure
- Lentiviral transduction on DIV1; axotomy on DIV7
- limitations
- Human protein was expressed in mouse neurons; injury model, not nutritional depletion or proof of human therapeutic benefit.
- nutrient_topic
- Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
- organism
- Human construct in mouse neurons
- plain_language
- The catalytic mutant spared axonal NAD after experimental nerve injury.
- primary_references
- [b3-cons-sarm2017] The SARM1 Toll/Interleukin-1 Receptor Domain Possesses Intrinsic NAD+ Cleavage Activity that Promotes Pathological Axonal Degeneration. (2017). https://pubmed.ncbi.nlm.nih.gov/28334607/ DOI: 10.1016/j.neuron.2017.02.022
- tissue_or_cell_type
- Cultured dorsal-root-ganglion axons
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 733–745
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstitution of Sarm1-null E13.5 mouse DRG neurons with SARM1 constructs · source_derived_draft · unverified_draft
### b3-cons-sarm-axotomy-nad After axotomy of Sarm1-null mouse DRG neurons, re-expression of active human SARM1 restored rapid axonal NAD+ depletion, whereas E642A did not. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The catalytic mutant spared axonal NAD after experimental nerve injury. organism: Human construct in mouse neurons tissue_or_cell_type: Cultured dorsal-root-ganglion axons experimental_model: Reconstitution of Sarm1-null E13.5 mouse DRG neurons with SARM1 constructs limitations: Human protein was expressed in mouse neurons; injury model, not nutritional depletion or proof of human therapeutic benefit. exposure: Lentiviral transduction on DIV1; axotomy on DIV7 cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 29", "start_char": 20432, "end_char": 22775, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "e75c162a4b5f51b7e6ef5e20612ed8ebfbe035a41abf81284cb055dfcf860333"} [b3-cons-sarm2017] The SARM1 Toll/Interleukin-1 Receptor Domain Possesses Intrinsic NAD+ Cleavage Activity that Promotes Pathological Axonal Degeneration. (2017). https://pubmed.ncbi.nlm.nih.gov/28334607/ DOI: 10.1016/j.neuron.2017.02.022
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.