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SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin
TLDR
The human SIRT6 protein is an NAD+-dependent, histone H3 lysine 9 (H3K9) deacetylase that modulates telomeric chromatin and contributes to the propagation of a specialized chromatin state at mammalian telomeres, which in turn is required for proper telomere metabolism and function.
Metformin improves healthspan and lifespan in mice
TLDR
It is shown that long-term treatment with metformin starting at middle age extends healthspan and lifespan in male mice, while a higher dose (1% w/w) was toxic.
Human RecQ helicases in DNA repair, recombination, and replication.
TLDR
Future research goals in this field include a better understanding of the division of labor among the human Rec Q helicases and learning how human RecQ helicases collaborate and cooperate to enhance genome stability.
Telomere-binding Protein TRF2 Binds to and Stimulates the Werner and Bloom Syndrome Helicases*
TLDR
In human cells, it is reported that WRN co-localizes and physically interacts with the critical telomere maintenance protein TRF2, and this interaction is mediated by the RecQ conserved C-terminal region of WRN.
The Bloom's and Werner's syndrome proteins are DNA structure-specific helicases
TLDR
It is shown that neither BLM nor WRN is capable of unwinding duplex DNA from a blunt-ended terminus or from an internal nick, and conclusively that a single-stranded 3'-tail is not a structural requirement for unwinding of standard B-form DNA by these helicases.
p53 modulation of TFIIH–associated nucleotide excision repair activity
TLDR
It is found that wild–type, but not Arg273His mutant p53 inhibits XPD (Rad3) and XPB DNA helicase activities and repair of UV–induced dimers is slower in Li–Fraumeni syndrome cells (heterozygote p53 mutant) than in normal human cells, indicating that p53 may play a direct role in modulating nucleotide excision repair pathways.
Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease
TLDR
Evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models is provided, suggesting that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis and thatMitophagy represents a potential therapeutic intervention.
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