Extended Data Fig. 9: Tri-1 and auranofin do not affect p16 and p53 signatures in aged mouse ovaries. | Nature Aging

Extended Data Fig. 9: Tri-1 and auranofin do not affect p16 and p53 signatures in aged mouse ovaries.

From: TXNRD1 drives the innate immune response in senescent cells with implications for age-associated inflammation

Extended Data Fig. 9

a, Heatmap of the SASP genes that were significantly upregulated in ovaries from aged mice (22 months) compared with young mice (4 months) (n = 10 biologically independent mice in young group, n = 9 biologically independent mice in aged group). b, Heatmap of the SASP genes that were significantly suppressed by Tri-1 treatment in aged mouse ovaries (n = 4 biologically independent mice per group). c-e, Ingenuity Pathway Analysis of the 1920 genes that were significantly different in aged vs young mice ovaries. Common gene expression changes induced by Tri-1 and auranofin treatments showed expected common inhibition of GSR and TXNRD1 regulators (c). Transcription factors with altered activity were listed with p53 and p16 among them (d). P values were calculated by a Fisher Exact Test estimated by Ingenuity Pathway Analysis Software. Both these two age-associated signatures were not affected with either Tri-1 or auranofin treatment in the aged mice (e). P values were calculated by hypergeometrical test.

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