Component

Human SARM1 TIR-domain construct

Experimentally expressed human SARM1 TIR fragment, residues 559–724; separate from full-length protein.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Purified human SARM1 TIR domain cleaved NAD+, producing ADP-ribose and nicotinamide as major products.

    Human SARM1 TIR-domain construct → NAD+ source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_span
    {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 24", "start_char": 15550, "end_char": 16946, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "9a9b91a772186c34d8b6305a04bbcf6d3acc40b0448e6f478811527c5174981e"}
    experimental_model
    Purified human SARM1 TIR domain; HPLC and LC-MS/MS
    exposure
    NAD+ incubation
    limitations
    Purified engineered TIR fragment rather than basal activity of intact full-length SARM1; no dietary dose inference.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Human
    plain_language
    SARM1 contains a catalytic domain that breaks NAD.
    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
    Cell-free preparation

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 677–689

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human SARM1 TIR domain; HPLC and LC-MS/MS · source_derived_draft · unverified_draft

    ### b3-cons-sarm-adpr-nam Purified human SARM1 TIR domain cleaved NAD+, producing ADP-ribose and nicotinamide as major products. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: SARM1 contains a catalytic domain that breaks NAD. organism: Human tissue_or_cell_type: Cell-free preparation experimental_model: Purified human SARM1 TIR domain; HPLC and LC-MS/MS limitations: Purified engineered TIR fragment rather than basal activity of intact full-length SARM1; no dietary dose inference. exposure: NAD+ incubation cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 24", "start_char": 15550, "end_char": 16946, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "9a9b91a772186c34d8b6305a04bbcf6d3acc40b0448e6f478811527c5174981e"} [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

  2. Human SARM1 TIR-domain NAD+ cleavage also generated cyclic ADP-ribose as a minor product.

    Human SARM1 TIR-domain construct → Cyclic ADP-ribose source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_span
    {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 24", "start_char": 15550, "end_char": 16946, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "9a9b91a772186c34d8b6305a04bbcf6d3acc40b0448e6f478811527c5174981e"}
    experimental_model
    Purified human SARM1 TIR domain; HPLC and LC-MS/MS
    exposure
    NAD+ incubation
    limitations
    Purified engineered TIR fragment rather than basal activity of intact full-length SARM1; no dietary dose inference. Drosophila product ratios differed and are not generalized to humans.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Human
    plain_language
    The human SARM1 reaction also makes some cyclic ADP-ribose.
    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
    Cell-free preparation

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 691–703

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human SARM1 TIR domain; HPLC and LC-MS/MS · source_derived_draft · unverified_draft

    ### b3-cons-sarm-cadpr Human SARM1 TIR-domain NAD+ cleavage also generated cyclic ADP-ribose as a minor product. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The human SARM1 reaction also makes some cyclic ADP-ribose. organism: Human tissue_or_cell_type: Cell-free preparation experimental_model: Purified human SARM1 TIR domain; HPLC and LC-MS/MS limitations: Purified engineered TIR fragment rather than basal activity of intact full-length SARM1; no dietary dose inference. Drosophila product ratios differed and are not generalized to humans. exposure: NAD+ incubation cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 24", "start_char": 15550, "end_char": 16946, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "9a9b91a772186c34d8b6305a04bbcf6d3acc40b0448e6f478811527c5174981e"} [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

What acts on it

  1. Nicotinamide inhibited purified human SARM1 TIR NADase activity, with an assay IC50 of 43.8 micromolar.

    Nicotinamide → Human SARM1 TIR-domain construct source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_span
    {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 25", "start_char": 16947, "end_char": 18260, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "bf110010a793c4d1d3c263db9f213aa5d539bcf1501265fe30fb1ab9ed4028fa"}
    experimental_model
    Purified domain dose-response assay
    exposure
    Nicotinamide titration; starting NAD+ about 5 micromolar
    limitations
    Purified engineered TIR fragment rather than basal activity of intact full-length SARM1; no dietary dose inference. IC50 depends on assay conditions and is not a therapeutic plasma target.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Human
    plain_language
    A product of NAD cleavage fed back to inhibit the isolated SARM1 domain.
    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
    Cell-free preparation

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 705–717

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified domain dose-response assay · source_derived_draft · unverified_draft

    ### b3-cons-nicotinamide-sarm-inhibition Nicotinamide inhibited purified human SARM1 TIR NADase activity, with an assay IC50 of 43.8 micromolar. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A product of NAD cleavage fed back to inhibit the isolated SARM1 domain. organism: Human tissue_or_cell_type: Cell-free preparation experimental_model: Purified domain dose-response assay limitations: Purified engineered TIR fragment rather than basal activity of intact full-length SARM1; no dietary dose inference. IC50 depends on assay conditions and is not a therapeutic plasma target. exposure: Nicotinamide titration; starting NAD+ about 5 micromolar cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 25", "start_char": 16947, "end_char": 18260, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "bf110010a793c4d1d3c263db9f213aa5d539bcf1501265fe30fb1ab9ed4028fa"} [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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards