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. 2010 Aug 13;5(8):e12173. doi: 10.1371/journal.pone.0012173

Figure 6. Working model depicting regulation of CREB and ATF1 on ATM/CK cluster residues.

Figure 6

Both proteins are constitutively phosphorylated on CK residues resulting in CREB-4P and ATF1-5P isoforms that are further phosphorylated in response to DNA damage on Ser-121 and Ser-51, respectively to yield CREB-5P and ATF1-6P isoforms. Phosphorylation of CREB CK residues (Ser-108/111/114/117) is stimulated by a CM factor, whereas ATF1 CK residues (Ser-36/38/41/44/47) are constitutively phosphorylated (indicated by bold arrow). PP2A/B56γ antagonizes phosphorylation of ATM sites in both CREB and ATF1. Inhibition of CBP binding is one endpoint of ATM/CK cluster phosphorylation. The dashed line denotes that phosphorylation of CK sites in ATF1 is sufficient to inhibit CBP binding in the absence of DNA damage.