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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