Research Paper Volume 15, Issue 19 pp 9984—10009

Figure 5. Normal behavior of BMAL1 in driving transcription in non-senescent cells is lost in favor of narrow binding to AP-1 binding sites in senescence, and in a senescent context BMAL1 mediates expression of AP-1 target genes conferring resistance to apoptosis. This highlights a previously unappreciated role of the core circadian clock component BMAL1 on the molecular phenotype of senescent cells.