Fig. 2.

Summary of interactions leading to NF-κB activation in C85 cells during maintenance phase of methotrexate-induced senescence. Listed are selected molecules upregulated in senescent C85 cells whose functional assignment was performed in IPA software. AKT protein kinase B; AREG amphiregulin; Bcl-xL BCL2-like 1 nuclear gene encoding mitochondrial protein (BCL2L1); BIRC3 baculoviral IAP repeat-containing 3 apoptosis inhibitor; BMP1/2 bone morphogenetic protein 1/2; CXCL1/3 chemokine ligand 1/3; DR3/4/5/6 death receptor 3/4/5/6; EREG epiregulin; FAS TNF receptor superfamily, member 6; ICAM1 intracellular adhesion molecule 1; IKBKG inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase gamma; iNOS inducible nitric oxide synthase (NOS2A); LTBR lymphotoxin beta receptor; NFKB2 nuclear factor of kappa light polypeptide gene enhancer in B-cells 2; NIK NFKB-inducing kinase; NRG1 neuregulin 1; PDGFA platelet-derived growth factor alpha; PLAT tissue plasminogen activator; RANTES chemokine ligand 5; RELB v-rel reticuloendotheliosis viral oncogene homolog B; TAB2 MAP3K7-interacting protein 2; TAK1 TGF beta-activated kinase 1 (MAP3K7); TGFA transforming growth factor alpha; TWEAK-R TNF receptor superfamily member 12A. Corresponding microarray data are presented in Table S5