Nevertheless, how p53 modulates TIME is still elusive ... In addition, IL-34 exposure resulted in noteworthy increased CD36 expression, causing the TAMs to polarize toward the pro-tumoral phenotype.

The scientists fused the target binding sequence to a reporter with strong expression to assess if p53 could repress its transcription. When the results didn’t show any reduction in gene expression, ...

New research uncovers new insights into preventing chronic inflammation caused by aging-related zombie-like cells. In humans ...

p53 enhances DNA repair and suppresses cytoplasmic chromatin fragments and inflammation in senescent cells - ...

New findings show that the mitochondria powering our cells also control the ability of a DNA repair protein to suppress the senescence-associated secretory phenotype (SASP), which causes zombie-like ...

Figure 8: Regulation of ALDH3A1 and NECTIN4 by p53. Researchers Jessica J. Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J. Munoz, and Fred Bunz from the Sidney ...

No one really understands why activation of the tumor suppressor p53 sometimes leads to cell-cycle arrest and sometimes induces an apoptotic program. It has been proposed that post-translational ...

One such mechanism involves a protein called p53. Often dubbed the "guardian of the genome," this protein plays a pivotal role in ensuring that your cells grow, divide and die in an orderly fashion.

A new research paper was published in Oncotarget, Volume 16, on February 18, 2025, titled "Robust p53 phenotypes and prospective downstream targets in telomerase-immortalized human cells.