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. 2022 Oct 27;13(2):432–453. doi: 10.1158/2159-8290.CD-22-0528

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©2022 The Authors; Published by the American Association for Cancer Research

This open access article is distributed under the Creative Commons Attribution 4.0 International (CC BY 4.0) license.

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Figure 4. — Senescent cells are primed to sense and amplify IFNγ signaling. A and B, IFNGR1 level on proliferating and senescent cells profiled by mass spectrometry (A) and validated by flow cytometry (B). AU, arbitrary unit. Data are presented as mean ± SEM. n = 6 for both the proliferating and senescent groups. C, Transcriptomic analysis of selected genes regulating IFNγ signaling from RNA-seq data of 3 independent p53-restorable cell lines (NSP, NSM2, and NSP5) restoring p53 along with NSP cells treated with two other senescence triggers. SEN/PRO, senescent/proliferating; T + P, trametinib plus palbociclib. D, mRNA expression of selected genes involved in IFNγ signaling in human cell lines triggered to senesce. Treatment: Ali, alisertib; Eto, etoposide; number indicates the length of treatment (days). Data are obtained from the public dataset SENESCopedia (44). E, Top, immunoblot analysis of NSP cells under different senescent triggers in the presence or absence of IFNγ (1 ng/mL). Bottom, quantification of the intensity of signal from immunoblot. p-STAT1, phospho-STAT1 (Tyr701).