SPTP_SALTY Effector proteins function to alter host cell physiology and promote bacterial survival in host tissues. This protein includes tyrosine phosphatase and GTPase activating protein (GAP) activities. After bacterial internalization, GAP mediates the reversal of the cytoskeletal changes induced by SopE. This function is independent of its tyrosine phosphatase activity, which remains unclear.[1][2][3]
Evolutionary Conservation
Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf.
↑Kaniga K, Uralil J, Bliska JB, Galan JE. A secreted protein tyrosine phosphatase with modular effector domains in the bacterial pathogen Salmonella typhimurium. Mol Microbiol. 1996 Aug;21(3):633-41. PMID:8866485
↑Fu Y, Galan JE. A salmonella protein antagonizes Rac-1 and Cdc42 to mediate host-cell recovery after bacterial invasion. Nature. 1999 Sep 16;401(6750):293-7. PMID:10499590 doi:https://dx.doi.org/10.1038/45829
↑Stebbins CE, Galan JE. Modulation of host signaling by a bacterial mimic: structure of the Salmonella effector SptP bound to Rac1. Mol Cell. 2000 Dec;6(6):1449-60. PMID:11163217
