Fig. 7.

Mechanistic model of the TE7 cell response to H₂O₂ and to H₂O₂ plus ATF2 knockdown. (A) H₂O₂ exposure causes DNA damage and consequently the activation of ATF2 via phosphorylation on threonine residues 69 and 71. This transcription factor induces the transcription of p21^WAF1 and c-Jun. As ATF2 induces the G2/M growth arrest via p21^WAF1, ATF2 thereby inhibits apoptosis. (B) The combination of H₂O₂ stress with the knockdown of ATF2 leads to reduced ATF2 protein level, causing a lesser amount of c-Jun and, most notably, of p21^WAF1. Consequently, G2/M arrest is reduced, but apoptosis reinforced.