| Autor: |
Murphy, Michaela E., Narasimhan, Akilavalli, Adrian, Alexis, Kumar, Ankur, Green, Cara L., Soto-Palma, Carolina, Henpita, Chathurika, Camell, Christina, Morrow, Christopher S., Yeh, Chung-Yang, Richardson, Claire E., Hill, Cristal M., Moore, Darcie L., Lamming, Dudley W., McGregor, Eric R., Simmons, Heather A., Pak, Heidi H., Bai, Hua, Denu, John M., Clark, Josef |
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| Zdroj: |
GeroScience; Feb2022, Vol. 44 Issue 1, p39-52, 14p |
| Abstrakt: |
As the aging population on a global and national scale reaches ever increasing highs, research is essential to reduce the burden of aging and age-related diseases. I Vav-iCre i SP ± sp I ;Ercc1 i SP I -/fl i sp mice are healthy into adulthood, but then display premature onset of immunosenescence characterized by senescence of specific immune cell populations and impaired immune function, similar to changes that occur with aging in wild-type mice. B Dr. Claire Richardson b , University of Wisconsin-Madison, investigated how aging affects neuron cell biology by exploiting the ability of the nematode I Caenorhabditis i elegans to de-couple the symptoms of aging from chronological age [[61]]. They discovered that morphological aging is cell-intrinsically controlled by focusing on features of neuron morphological aging. LSD1 also targets non-histone proteins p53 and RelA/p65, which contribute to senescence and the secretory phenotype of senescent cells (senescence-associated secretory phenotype or SASP). [Extracted from the article] |
| Databáze: |
Complementary Index |
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