“For the first time, the present study revealed a critical role for protein palmitoylation in the development of a DNA damage-induced senescence phenotype.”
BUFFALO, NY- September 10, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as “Aging (Albany NY)” and “Aging-US” by Web of Science), Volume 16, Issue 16 on August 23, 2024, entitled, “2-Bromopalmitate treatment attenuates senescence phenotype in human adult cells – possible role of palmitoylation.”
As noted in the Abstract of the paper, cells may undergo senescence in response to DNA damage, which is associated with cell cycle arrest, altered gene expression and altered cell morphology. Protein palmitoylation is one of the mechanisms by which the DNA damage response is regulated.
Researchers Adam Krzystyniak, Agata Gluchowska, Agata Pytyś, Magdalena Dudkowska, Tomasz Wójtowicz, Alicja Targonska, Dorota Janiszewska, Ewa Sikora, and Grazyna Mosieniak from the Nencki Institute of Experimental Biology in Warsaw, Poland, hypothesized that protein palmitoylation played a role in regulation of the senescent phenotype. They showed that treatment of senescent human vascular smooth muscle cells (VSMCs) with 2-bromopalmitate (2-BP) – an inhibitor of protein acyltransferases – is associated with changes in different aspects of the senescent phenotype, including the resumption of cell proliferation, a decrease in DNA damage markers and the downregulation of senescence-associated β-galactosidase activity.
“Our data suggest that cell senescence may be regulated by palmitoylation, which provides a new perspective on the role of this posttranslational modification in age-related diseases.”
Continue reading: DOI: https://doi.org/10.18632/aging.206080
Corresponding authors: Grazyna Mosieniak – [email protected], and Adam Krzystyniak – [email protected]
Keywords: aging, cell senescence, vascular smooth muscle cell, palmitoylation, 2-BP, DNA damage
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