Fig. 2

1 IpgB mediated to the block actin formation around vacuole. 2 IpaJ inhibit vesicle trafficking. 3 VirA lead to the disrupt of trafficking from RE to the Golgi and also mediated stabilized Rab1 in an inactivated form. 4 PIP5 regulate endosomal maturation and actin rearrangement and protect vacuole from lysosome degradation. 5 and 6 P62 can bind to the LC3 and also bind to the ubiquitin. 7 IpgB can mimic the role of RhoG and finally lead to the actin polymerization, massive recurrent of Rab11 to the vacuole. 8 PIP5 can activate Akt that mediated cell to survive. 9 TOM1 lead to lagging EGFR degradation. 10 IpgD can inhibit ATP releasing by cell as an inflammatory signal. 11 ICAM as a leukocyte receptor affected by IpgD and mediated to the internalization and degradation. 12 TOM1 inhibit vacuole maturation. IpaB, invasion plasmid antigen B; IpaJ, cysteine protease; IpgB, effector protein involved in Shigella invasion of host cells; IpaH, invasion plasmid antigen H gene sequence; Rab, Ras-related protein in brain; TOM 1, target of myb-1; RhoG, Ras homology growth related; ELMO, engulfment and cell motility protein; Dock180, dedicator of cytokinesis; ICAM, intercellular adhesion molecule; Akt, protein kinase B