Fig. 8: Models highlighting the role of CUX1 in mediation of cellular senescence by activation of p16INK4a expression.
From: Post-GWAS functional analysis identifies CUX1 as a regulator of p16INK4a and cellular senescence
a, The mechanism underlying the contribution of atherosclerosis-associated fSNP rs1537371 to susceptibility to age-related disease. Increased binding of CUX1 to the A allele (risk allele) versus the C allele (nonrisk allele) resulted in a higher level of p16INK4a expression which, in turn, augments senescence. b, The mechanism underlying the contribution of the CUX1/p16INK4a pathway to cellular senescence. Increased expression of CUX1 in response to telomere shortening, DNA damage and oxidative stress resulted in upregulated expression of p16INK4a and induction of cellular senescence.
