Results 221 to 230 of about 77,771 (318)

Exceptional Longevity Modifying Allele APOE2 Promotes DNA Signaling Pathways Resisting Cellular Senescence in Human Neurons

open access: yesAging Cell, Volume 25, Issue 5, May 2026.
Neurons expressing APOE2 were more resistant to endogenous DNA damage, activated transcriptional signaling pathways associated with DNA repair, and were resilient to stress‐induced DNA damage and cellular senescence. In contrast, APOE4 neurons exhibited elevated expression of rRNA repetitive elements and were prone to becoming senescent.
Cristian Gerónimo‐Olvera   +20 more
wiley   +1 more source

Cryo-electron microscopy structure of the budding yeast telomerase holoenzyme. [PDF]

open access: yesScience
Hu H   +6 more
europepmc   +1 more source

HOT1 is a mammalian direct telomere repeat-binding protein contributing to telomerase recruitment [PDF]

open access: bronze, 2013
Dennis Kappei   +15 more
openalex   +1 more source

Telomere Dysfunction and Proteostasis Decline Define Distinct Pathways of Cellular Senescence in the Human Respiratory Tract

open access: yesAging Cell, Volume 25, Issue 5, May 2026.
Telomere shortening occurs with age in the respiratory epithelium, but telomere dysfunction‐induced foci (TIF) accumulate only late in life. In contrast, proteostasis decline emerges earlier and correlates with functional impairment, suggesting it may be a primary driver of cellular senescence during physiological aging.
Céline Coquette   +20 more
wiley   +1 more source

Rare genetic diseases associated with G-quadruplex-induced replication stress. [PDF]

open access: yesCommun Biol
Herr LM   +6 more
europepmc   +1 more source

Long‐Term Stress Adaptation as a Highly‐Conserved Key Factor in Yeast Aging

open access: yesAging Cell, Volume 25, Issue 5, May 2026.
This study shows that long‐term, but not short‐term, stress exposure triggers molecular changes in yeast that mirror established hallmarks of aging, including altered proteostasis, epigenetic shifts, and reduced lifespan. These changes are reversible upon stress removal, and the genes involved are conserved across all domains of life. ABSTRACT Aging is
Yanzhuo Kong   +7 more
wiley   +1 more source

SIRT1 Downregulation by Advanced Glycation End Products Activates RANKL‐Dependent Osteoclast Signaling and Drives Chondrocyte Senescence During Osteoarthritis Development

open access: yesAging Cell, Volume 25, Issue 5, May 2026.
Mechanistic study of AGEs‐induced OA progression via SIRT1/RANKL/RANK signaling‐mediated osteoclast–chondrocyte communication and cellular senescence. ABSTRACT Advanced glycation end products (AGEs) accumulate with aging and metabolic stress and are increasingly implicated in osteoarthritis (OA) pathology.
Yizhou Li   +4 more
wiley   +1 more source

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