Component

Mouse nuclear NMNAT1

Context-specific entity; species, compartment and exposure are stated on each claim.

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.

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. Nmnat1 knockdown reduced PARP1-mediated PARylation in mouse 3T3-L1 preadipocytes; catalytically active but not inactive NMNAT1 rescued the activity.

    Mouse nuclear NMNAT1 → Mouse PARP1 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse shRNA and enzyme re-expression experiments.
    limitations
    PARP activity is not a direct measurement of all nuclear NAD-dependent reactions.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    DNA-associated enzymes can depend on local NAD production.
    primary_references
    Metabolic regulation of transcription through compartmentalized NAD+ biosynthesis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29748257/ · DOI 10.1126/science.aan5780
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 60–66

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse shRNA and enzyme re-expression experiments. · source_derived_draft · unverified_draft

    ## nad-plus-nmnat1-loss DNA-associated enzymes can depend on local NAD production. Nmnat1 knockdown reduced PARP1-mediated PARylation in mouse 3T3-L1 preadipocytes; catalytically active but not inactive NMNAT1 rescued the activity. Model: Mouse shRNA and enzyme re-expression experiments. Limitations: PARP activity is not a direct measurement of all nuclear NAD-dependent reactions. Evidence access: Primary full text Metabolic regulation of transcription through compartmentalized NAD+ biosynthesis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29748257/ · DOI 10.1126/science.aan5780
    Complete structured claim and evidence

What acts on it

  1. Adipogenic induction of cytoplasmic NMNAT2 in mouse 3T3-L1 cells competed with nuclear NMNAT1 for NMN and reduced nuclear NAD+ availability.

    Mouse NMNAT2 → Mouse nuclear NMNAT1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse preadipocyte differentiation, enzyme perturbations and compartment measurements.
    limitations
    Not evidence that human NMN supplements cause weight gain; enzyme location and differentiation state matter.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    Two compartments can compete for the same building material.
    primary_references
    Metabolic regulation of transcription through compartmentalized NAD+ biosynthesis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29748257/ · DOI 10.1126/science.aan5780

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 52–58

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse preadipocyte differentiation, enzyme perturbations and compartment measurements. · source_derived_draft · unverified_draft

    ## nad-plus-nmnat2-competition Two compartments can compete for the same building material. Adipogenic induction of cytoplasmic NMNAT2 in mouse 3T3-L1 cells competed with nuclear NMNAT1 for NMN and reduced nuclear NAD+ availability. Model: Mouse preadipocyte differentiation, enzyme perturbations and compartment measurements. Limitations: Not evidence that human NMN supplements cause weight gain; enzyme location and differentiation state matter. Evidence access: Primary full text Metabolic regulation of transcription through compartmentalized NAD+ biosynthesis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29748257/ · DOI 10.1126/science.aan5780
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In mouse preadipocytes, PARP1-dependent ADP-ribosylation repressed C/EBP beta adipogenic transcription; reduced nuclear NAD synthesis relieved this repression.

    Mouse PARP1 → Mouse C/EBP beta / Cebpb source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse 3T3-L1 transcription and differentiation experiments.
    limitations
    Cell differentiation mechanism, not a universal whole-body fat response.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    A local NAD change can alter a gene program through protein modification.
    primary_references
    Metabolic regulation of transcription through compartmentalized NAD+ biosynthesis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29748257/ · DOI 10.1126/science.aan5780

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 68–74

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse 3T3-L1 transcription and differentiation experiments. · source_derived_draft · unverified_draft

    ## nad-plus-parp-cebpb A local NAD change can alter a gene program through protein modification. In mouse preadipocytes, PARP1-dependent ADP-ribosylation repressed C/EBP beta adipogenic transcription; reduced nuclear NAD synthesis relieved this repression. Model: Mouse 3T3-L1 transcription and differentiation experiments. Limitations: Cell differentiation mechanism, not a universal whole-body fat response. Evidence access: Primary full text Metabolic regulation of transcription through compartmentalized NAD+ biosynthesis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29748257/ · DOI 10.1126/science.aan5780
    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