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Table 3 Pathogens and actin interaction

From: A glance on the role of actin in osteogenic and adipogenic differentiation of mesenchymal stem cells

Pathogen Mechanism of action adaptation in host cell References
Salmonella spp. Translocate effectors (SopE and SopE2) into host cells which increase F actin polymerization. [133, 134, 137]
Listeria monocytogenes ActA protein recruits an Arp2/3 on the surface of listeria which promotes actin polymerization that helps in the movement of bacteria in the cells. [139, 140]
E. coli Actin-rich filament that facilitates their attachment. [141, 142]
Chlamydia trachomatis Secrete actin-recruiting phosphoprotein (Tarp) which cause actin polymerization depolymerization in the host cell. [143, 144]
Coxiella burnetii Infects phagocytic human macrophages via binding to complement receptor 3 (CR3) receptors, triggering the reorganization of filamentous actin at the attachment site. [145]
Rickettsia conorii Attachment to host cell requires actin rearrangement via recruitment and activation of Arp2/3. [146]
Tick-borne pathogen Anaplasma phagocytophilu Actin polymerization at invasion. [147]
Ehrlichia chaffeensis Manipulation of cytoskeleton through SUMOylation-dependent protein-protein interactions between bacterial effectors and host cytoskeletal components. [148]
Vaccinia viruses Receptor tyrosine kinase signaling which in turn ignite actin polymerization through N-WASP-Arp2/3 cascade. [149]