FEATURES

FAMILY

DESCRIPTION

Also known as INLC_LISMG, inlC, irpA. A virulence enhancer that has at least 2 dissociable functions in infection; it impairs translocation of host transcription factor NF-kappa-B to the nucleus and antagonizes the function of the Tuba dynamin-binding protein, promoting bacterial spreading (PubMed:20855622, PubMed:19767742, PubMed:24332715). Perturbs the morphology of host cell junctions by impairing host DNMBP (Tuba) and WASL interaction, altering cortical tension at the cell junctions and allowing bacteria to more efficiently form bacteria-filled cell protrusions which promote bacterial spreading within infected host tissue (PubMed:19767742, PubMed:24332715). Down-regulates the host inflammation response usually induced by Listeria infection. Interacts with host I-kappa-B kinase alpha (IKKA, CHUK), which prevents IKKA from phosphorylating NF-kappa-B inhibitor alpha (IKBA, NFKBIA) and thus delays degradation of phospho-IKBA. Translocation of host transcription factor p65 (a subunit of NF-kappa-B, RELA) into the nucleus is impaired, which prevents activation of NF-KB-regulated genes (PubMed:20855622). Recognized by serum from healthy humans exposed to L.monocytogenes as well from patients who have recovered from listeriosis (PubMed:9284184). Interacts in vitro with human intestinal mucin-2 (MUC2) but not with mucin-1; binding is slightly better at pH 5.5, (the pH of the intestine) than at pH 7.4 (PubMed:18327567). Interacts with the SH3 6 domain of human DNMBP (Tuba) (PubMed:19767742, PubMed:24332715). Interacts with I-kappa-B kinase alpha (IKKA, CHUK) (PubMed:20855622).

EXTERNAL LINKS

inlC

Mutations

Mutation(s) distribution

Mutations table