Lifespan. David Sinclair
Читать онлайн книгу.
D. Mills, D. A. Sinclair, and L. Guarente, “MEC1-Dependent Redistribution of the Sir3 Silencing Protein from Telomeres to DNA Double-Strand Breaks,”
65
Sinclair, Mills, and Guarente, “Accelerated Aging and Nucleolar Fragmentation in Yeast SGS1 Mutants.”
66
P. Oberdoerffer, S. Michan, M. McVay, et al., “SIRT1 Redistribution on Chromatin Promotes Genomic Stability but Alters Gene Expression During Aging,”
67
A. Ianni, S. Hoelper, M. Krueger, et al., “Sirt7 Stabilizes rDNA Heterochromatin Through Recruitment of DNMT1 and Sirt1,”
68
The authors show how SIRT7, in protecting against the instability of rDNA, also guards against the death of human cells. S. Paredes, M. Angulo-Ibanez, L. Tasselli, et al., “The Epigenetic Regulator SIRT7 Guards Against Mammalian Cellular Senescence Induced by Ribosomal DNA Instability,”
69
Oberdoerffer et al., “SIRT1 Redistribution on Chromatin Promotes Genomic Stability but Alters Gene Expression During Aging.”
70
M. W. McBurney, X. Yang, K. Jardine, et al., “The Mammalian SIR2alpha Protein Has a Role in Embryogenesis and Gametogenesis,”
71
R.-H. Wang, K. Sengupta, L. Cuiling, et al., “Impaired DNA Damage Response, Genome Instability, and Tumorigenesis in SIRT1 Mutant Mice,”
72
R. Mostoslavsky, K. F. Chua, D. B. Lombard, et al., “Genomic Instability and Aging-like Phenotype in the Absence of Mammalian SIRT6,”
73
The treatments work better in male mice, for reasons that are not yet known, but my former postdoc Haim Cohen at Bar-Ilan University in Israel wins the award for the best-ever name given to a transgenic mouse strain: MOSES. A. Satoh, C. S. Brace, N. Rensing, et al., “Sirt1 Extends Life Span and Delays Aging in Mice Through the Regulation of Nk2 Homeobox 1 in the DMH and LH,”
74
When we write
75
It’s possible that by not allowing mating-type genes to turn on, yeast with additional copies of
76
M. G. L. Baillie,
77
Along with bristlecones, Matthew LaPlante, my coauthor on
78
When researchers compared trees of a variety of ages to look for a steady incremental decline in annual shoot growth, they found “no statistically significant age-related differences.” R. M. Lanner, and K. F. Connor, “Does Bristlecone Pine Senesce?,”
79
Investigating mutations in the gene Daf-2, researchers made a remarkable find: the largest reported lifespan extension of any living thing, namely twice as long. This relied on the involvement of two genes, Daf-2 and Daf-16, opening the door to new horizons of ways to understand how to prolong life. C. Kenyon, J. Chang, E. Gensch, et al., “A
80
Why do genes often have a variety of names? The language of genetics is just like any other language; its words contain the echoes of history. Knowing the entire genome of a yeast cell, a nematode worm, or a human was the stuff of dreams less than a quarter century ago. Now, of course, I can sequence my own genome in a day on a USB drive–sized sequencer. When I was a student, genes would be given a name based on the characteristics of mutants we would generate with mutagenic chemicals. Typically, all we knew about a gene when we named it was its rough location on a particular chromosome. Only later were its distant cousins identified.
81
A. Brunet, L. B. Sweeney, J. F. Sturgill, et al., “Stress-Dependent Regulation of FOXO Transcription Factors by the SIRT1 Deacetylase,”
82
O. Medvedik, D. W. Lamming, K. D. Kim, and D. A. Sinclair, “
83
The authors found convincing evidence linking
84
H. Bae, A. Gurinovich, A. Malovini, et al., “Effects of
85
If you’re a dedicated exerciser in middle age or an athlete in her fifties, chances are your heart is going to resemble that of someone much younger, several studies have revealed. Not so for the office worker who doesn’t exercise or someone who hits the gym or runs in the street on a sporadic basis. What isn’t clear, though, is whether commencing an aggressive exercise program in your middle years can turn around the effects of a sedentary lifestyle on the heart’s functioning and structure. G. Reynolds, “Exercise Makes the Aging Heart More Youthful,”
86
“These findings have implications for improving blood flow to organs and tissues, increasing human performance, and reestablishing a virtuous cycle of mobility in the elderly.” A. Das, G. X. Huang, M. S. Bonkowski, et al., “Impairment of an Endothelial NAD+-H2S Signaling Network Is a Reversible Cause of Vascular Aging,”