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Stutchman, Jeremy

A5042492824 | I157725225

Mayo Clinic

University of Illinois Urbana-Champaign

Citations 2

CHCHD2 mediates glioblastoma cell proliferation, mitochondrial metabolism, hypoxia‑induced invasion and therapeutic resistance

International Journal of Oncology | August 25, 2023 | Volume: 63 | Issue: 5 | Pages: No page available

10.3892/ijo.2023.5565 | PMID 37654190

p21 produces a bioactive secretome that places stressed cells under immunosurveillance

Science | October 28, 2021 | Volume: 374 | Issue: 6567 | Pages: No page available

10.1126/science.abb3420 | PMID 34709885

The clock is ticking for senescent cells Senescent cells promote their own recognition and removal through the immune system by generating a bioactive secretome called the senescence-associated secretory phenotype (SASP). Sturmlechner et al . report that the cell cycle regulator p21 directs an early form of the SASP, which they call the p21-activated secretory phenotype (PASP) (see the Perspective by Reen and Gil). As part of the PASP, the chemokine CXCL14 attracts macrophages, which monitor stressed cells expressing elevated p21. If stressed cells recuperate and p21 levels return to normal within 4 days, then macrophages disengage from their targets. Otherwise, macrophages recruit cytotoxic T cells that facilitate target cell removal. Other cell cycle regulators such as p16 can induce many factors overlapping with the PASP, but p21 uniquely drives this CXCL14-mediated “timer” mechanism of senescent cell immunosurveillance. —STS