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). Expression induced by PrfA; expressed in bacterial growth medium at very low levels in the absence of extra copies of prfA (at protein level) (PubMed:8878044, PubMed:8641748, PubMed:8975898). Transcription induced upon a shift to growth in minimal medium and also in infected mouse cells; expression is low 1 hour post-infection and reaches its maximum 5 hour post-infection (PubMed:8878044). Detected by 5 hours post infection in human Caco-2 cells (at protein level) (PubMed:19767742). In infected HeLa cells expression increases gradually over time (at protein level) (PubMed:20855622). Consists of the cap domain (residues 35-76) and LRR repeat region (77-213) and an Ig-like region (207-297), where the latter 2 overlap slightly (PubMed:17057330). The LRR repear region interacts via its concave face with host DNMBP (Tuba) (PubMed:24332715). Significant reduction in virulence when injected intravenously into C57BL/6 mice; no effect on intracellular growth of bacteria in infected cell lines (PubMed:8878044, PubMed:20855622, PubMed:23403554). Slightly reduced virulence when injected intravenously into BALB/c mice; no effect on intracellular growth of bacteria in infected cell lines (PubMed:8975898). Decreased bacterial spreading in polarized epithelial cells (human Caco-2 BBE1 cell line), decreased formation of host cell plasma membrane protusions, host cell junctions are not perturbed by bacteria (PubMed:19767742). Significantly increased production of cytokines, significantly increased recruitment of neutrophils to the peritoneum, after intraperitoneal injection into BALB/c mice (PubMed:20855622). In infected host cells Listeria surface protein ActA induces formation of F-actin 'comet tails' that propel bacteria. Motile bacteria ultimately encounter the host plasma membrane, deforming it into protrusions. Finally, pathogen-containing protrusions are engulfed by adjacent mammalian cells. Belongs to the internalin family. Conflicting results are seen for mutagenesis of Lys-173. It is seen to reduce binding to the SH3 6 domain of human DNMBP (Tuba) by surface plasmon resonance (PubMed:19767742). In the crystal structure with Tuba this reside is seen not to be in the protein-protein interface, and pull-down assays show it interacts normally with Tuba (PubMed:24332715). Two studies show this residue is important for virulence in the mouse model (PubMed:19767742, PubMed:23403554).