Tier 3 — preclinical

Lamin A Is an Endogenous SIRT6 Activator and Promotes SIRT6-Mediated DNA Repair

Shrestha Ghosh, Baohua Liu, Yi Wang, Quan Hao, Zhongjun Zhou
Cell Reports 2015 13(7):1396-1406

Bibliography

PubMed
PMID 26549451
DOI
10.1016/j.celrep.2015.10.006

Study snapshot

DesignMechanistic cellular and biochemical study.
ModelHuman cell systems examining lamin A/progerin regulation of SIRT6.
Sample
InterventionLamin A and progerin perturbation.
DurationExperimental.
EndpointsSIRT6 activation; SIRT6 chromatin recruitment; DNA-PKcs recruitment; CtIP deacetylation; PARP1 mono-ADP-ribosylation

What the study showed, in plain terms

Lamin A directly supports SIRT6 activity and helps recruit SIRT6 to damaged chromatin. Progerin, the abnormal lamin A protein in Hutchinson-Gilford progeria, disrupts this relationship and weakens SIRT6-dependent DNA-repair signaling.

Key findings

Lamin A acts as an endogenous SIRT6 activator and promotes multiple SIRT6-dependent DNA-repair events, while progerin compromises SIRT6 activation and recruitment.

What this study can and cannot tell us

This is mechanistic cellular evidence, not a human intervention showing that increasing lamin A or SIRT6 improves aging outcomes.

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Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability