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. 2013 Jul 22;110(32):E2950–E2957. doi: 10.1073/pnas.1307736110

Fig. 4.

Fig. 4.

Involvement of ATM signaling in mTORC1 repression following NO exposure. (A) Western analysis with p-ATM, p-CHK2, p-AMPK, and p-ACC antibodies and their total protein counterparts shows activation of ATM and downstream effectors in MCF-7 cells exposed to NO. (B) Western analysis of ATM+/+, ATM+/−, and ATM−/− MEF with p-S6K, p-S6, and p4E-BP1 antibodies shows that repression of mTORC1 by SN is ATM-dependent. (C) Western analysis of EBV-immortalized B-lymphocytes obtained from an AT (AT-B) patient and nonmutant individuals (WT-B) with p-ATM, p-S6K, and p-S6 antibodies shows that repression of mTORC1 by SN is ATM-dependent. (D) Western analysis with p-ATM, p-S6K, p-S6, and p4E-BP1antibodies and their total protein counterparts in HeLa (LKB1-null cells) shows that repression of mTORC1 by NO exposure is LKB1-dependent. (E) Western analysis with p-ATM, p-S6K, and pS6 antibodies in TSC2+/+ and TSC2−/− MEF shows that repression of mTORC1 by NO exposure is TSC2-dependent. CT, control.