Tier 3 — preclinical
SIRT6 links histone H3 lysine 9 deacetylation to NF-kappaB-dependent gene expression and organismal life span
Cell
2009
136(1):62-74
Bibliography
- PubMed
- PMID 19135889
- PubMed Central
- PMC2757125
- Funding
- NIH funding indexed by PubMed: NIA K08 AG028961, NIA R01 AG028867, and NCI R01 CA118750.
- Competing interests
- No competing-interest statement was identified in the accessible full-text record.
Study snapshot
| Design | Mechanistic genetic and chromatin-regulation study using SIRT6-deficient cells and mice. |
|---|---|
| Model | SIRT6-deficient and control mouse models plus cultured cells. |
| Sample | Preclinical experiments; sample sizes vary by assay and are reported in the full paper. |
| Intervention | Genetic SIRT6 deficiency and mechanistic interrogation of NF-kappaB signaling. |
| Duration | Experiment-dependent. |
| Endpoints | NF-kappaB target-gene expression; SIRT6 chromatin occupancy; H3K9 acetylation; premature-aging/lifespan phenotype |
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- SIRT6, Inflammation & LINE1: NF-κB, cGAS and InflammagingSIRT6 suppresses NF-kappaB genes and LINE1 retrotransposons in experimental models. See how cGAS signaling connects genome instability to inflammaging.Read analysis
- What Is SIRT6? Function, Aging, DNA Repair & Human EvidenceSIRT6 is an NAD+-dependent nuclear enzyme involved in DNA repair, chromatin, metabolism and aging. Mouse studies show lifespan effects; human studies now...Read analysis
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