First-pass extracted concept

NRF1

Candidate: concept label1 source documents5 linked claims

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Aliases

nuclear respiratory factor 1

Evidence Snippets

Here, we elucidate the pivotal role of nuclear respiratory factor 1 (NRF1) in orchestrating innate immune responses that drive senescence and the senescence-associated secretory phenotype (SASP).

Evidence 1Source 1DOI PubMedprovenance

Supporting Sources

Source 1primary paper2025MEDDOI PubMed

1 evidence snippet 5 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1mechanistic regulationsupports2025Source 1DOI PubMed

NRF1 enhances SASP by transcriptionally regulating TBK1 and IRF3.

Quoted textsource-backed

Mechanistically, NRF1 enhanced SASP by transcriptionally regulating TBK1 and IRF3, critical nodes in innate immunity essential for senescence induction.

Claim 2mechanistic rolesupports2025Source 1DOI PubMed

NRF1 orchestrates innate immune responses that drive senescence and SASP.

Quoted textsource-backed

Here, we elucidate the pivotal role of nuclear respiratory factor 1 (NRF1) in orchestrating innate immune responses that drive senescence and the senescence-associated secretory phenotype (SASP).

Claim 3perturbation effectsupports2025Source 1DOI PubMed

NRF1 deficiency delays cellular senescence and ameliorates age-related deterioration in multiple organs.

Quoted textsource-backed

NRF1 deficiency delayed cellular senescence and ameliorated age-related deterioration in multiple organs.

Claim 4perturbation effectsupports2025Source 1DOI PubMed

NRF1 deficiency suppresses innate immune activation and attenuates inflammation associated with senescence and aging.

Quoted textsource-backed

Conversely, NRF1 deficiency suppressed innate immune activation, thereby attenuating inflammation associated with senescence and aging.

Claim 5signaling mechanismsupports2025Source 1DOI PubMed

DNA damage activates ATM kinase, which phosphorylates NRF1 at Ser393 and augments the NRF1-TBK1/IRF3-type I interferon axis to exacerbate cellular senescence.

Quoted textsource-backed

Additionally, DNA damage activated ATM kinase, which phosphorylated NRF1 at Ser393, augmenting the NRF1-TBK1/IRF3-type I interferon axis and exacerbating cellular senescence.