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Table 1 A selection of upregulated genes in wildtype-infected cells compared to uninfected cells.

From: Microarray analysis of Shigella flexneri-infected epithelial cells identifies host factors important for apoptosis inhibition

Gene Function Fold Induction
Association with the inhibition of the extrinsic pathway of apoptosis
   TNFAIP3 aka A20; inhibits TNF-alpha-induced apoptosis by inhibiting caspase-8 cleavage 9.3
   TNFRSF12A functions, in part, through the NF-κB pathway to up-regulate BCL-XL and BCL-W expression for malignant cell survival 5.1
   CSE1L binds strongly to importin-alpha; highly expressed in tumor cell lines and may play a role in inhibiting TNF-mediated cell death 3.1
   FAIM3 Fas apoptotic inhibitory molecule 3; inhibits caspase-8 processing 2.7
   BAG4 associates with TNFR1 and death receptor-3 to negatively regulate downstream death signaling 2.6
   CFLAR CASP8 and FADD-like apoptosis regulator; aka c-FLIP; interacts with FADD and FLICE; inhibits apoptosis via human death receptors 2.5
   FAIM Fas apoptotic inhibitory molecule; pro-survival; mediates Fas resistance produced by surface Ig engagement in B cells 2.1
   PEA15 a death effector domain (DED)-containing protein; inhibits both TNFRSF6 and TNFRSF1A-mediated CASP8 activity & apoptosis 2.1
   TNFAIP8 tumor necrosis factor, alpha-induced protein 8; inhibits the activated form of caspase-8 2.1
Interaction with caspases (IAP genes)
   BIRC4 aka XIAP; inhibits apoptosis through binding to TRAF1 and TRAF2; also inhibits caspase-3 and caspase-7 3.5
   BIRC1 aka NAIP; homology to two baculoviral IAPs; suppresses apoptosis induced by various signals; binds caspase-9 3.2
   BIRC5 aka survivin; with hepatitis B X-interacting protein (HBXIP) binds caspase-9; variant DeltaEx3 binds caspase-3 with BCL-2 2.8
   BIRC7 aka livin; shown to interact with caspase-3, -7, & -9; degrades Smac/DIABLO 2.8