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. 2012 Feb 1;8(2):236–251. doi: 10.4161/auto.8.2.18600

Figure 4.

Figure 4

DNA damage induces sustained activation of AMPK and ULK1 in p18-CycE-expressing cells. (A and B) Cytoplasmic fractions of cells, at the indicated time following IR, were immunoblotted for ATM-ser1981, ATM, pAMPK-thr172, AMPK. β-actin was used as a loading control. (C and D) Total protein lysates of cells at the indicated time following IR were immunoblotted for pULK1-ser467, ULK1, and β-actin. (E) Total protein lysates of cells at 24 h following IR with or without 1 h pretreatment with the ATM inhibitor KU-55933 (10 µM) were immunoblotted for pULK1-ser467, ULK1, pAMPK-thr172, AMPK and β-actin. (F) Cytoplasmic fractions of cells at 6 h following IR with or without 1 h pretreatment with the ATM inhibitor KU-55933 (10 µM) were immunoblotted for ATM-ser1981 and ATM. (G) Total protein lysates of cells at 24 h following IR with or without 1 h pretreatment with the AMPK inhibitor Compound C (CC; 25 µM) were immunoblotted for pULK1-ser467, ULK1, pAMPK-thr172, AMPK and β-actin.