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The finding means that "it's inescapable that aging is regulated deliberately by genes," says Cynthia Kenyon, a molecular geneticist at the University of California, San Francisco.
Work by many researchers have shown that aging is regulated by key genes working in a network of signaling pathways and that there is no single gene or pathway that completely controls the aging process.
That said, most scientists believe that just as with other biological processes, aging is regulated by conserved signaling pathways.
Thus, aging is regulated by signaling networks encompassing nutrient-sensing, and mitogen-activated, stress-responsive and DDR signaling pathways.
Thus, genetic studies have now firmly established that aging is regulated by specific genes conserved from yeast to mice [ 23, 30- 34].
Aging is regulated by the extent of stochastic damage that accumulates over time and the rate at which this damage accumulates (Kirkwood & Holliday, 1979).
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However, how changes in Ets1/2 and ID protein expression during aging are regulated is still elusive.
These two types of aging are regulated by partially overlapping regulatory mechanisms.
The declines in SVZ proliferation, stem cell self-renewal potential, and neurogenesis during aging are regulated by a pathway that includes let-7 microRNAs, the chromatin-associated HMGA2 high mobility group protein, and the p16Ink4a cyclin-dependent kinase inhibitor: let-7b expression increases with age, reducing Hmga2 expression and increasing p16Ink4a expression (Nishino et al., 2008).
Understanding this plasticity may help us understand how ageing is regulated and is subject to external interventions.
Autophagy, a mechanism important in regulating stress response and aging is negatively regulated by mTOR [39], [40], whereas SIRT1 has been reported to activate autophagy by deacetylating several essential components of the autophagy machinery [41].
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