Title
The carboxyl-terminal SH3 domain of the mammalian adaptor CrkII promotes internalization of Listeria monocytogenes through activation of host phosphoinositide 3-kinase
Abbreviated Journal Title
Cell Microbiol.
Keywords
PHOSPHATIDYLINOSITOL 3-KINASE; TYROSINE-PHOSPHORYLATION; ACTIN; POLYMERIZATION; HELICOBACTER-PYLORI; SIGNALING PATHWAY; EPITHELIAL-CELLS; SURFACE PROTEIN; SMALL GTPASES; INIB PROTEIN; MET; RECEPTOR; Cell Biology; Microbiology
Abstract
The intracellular bacterial pathogen Listeria monocytogenes causes food-borne illnesses leading to gastroenteritis, meningitis or abortion. Listeria induces its internalization into some mammalian cells through binding of the bacterial surface protein InlB to its host receptor, the Met Receptor Tyrosine Kinase. InlB-induced activation of Met stimulates host signal transduction pathways that culminate in cell surface changes driving pathogen engulfment. One mammalian protein with the potential to couple Met to downstream signalling is the adaptor CrkII. CrkII contains an unusual carboxyl-terminal SH3 domain (SH3C) that promotes entry of Listeria. However, binding partners or downstream effectors of SH3C remain unknown. Here, we use RNA interference and overexpression studies to demonstrate that SH3C affects bacterial uptake, at least in part, through stimulation of host phosphatidylinositide (PI) 3-kinase. Experiments with latex beads coated with InlB protein indicated that one potential role of SH3C and PI 3 kinase is to promote changes in the F-actin cytoskeleton necessary for particle engulfment. Taken together, our results indicate that the CrkII SH3C domain engages a cellular ligand that regulates PI 3 kinase activity and host cell surface rearrangements.
Journal Title
Cellular Microbiology
Volume
9
Issue/Number
10
Publication Date
1-1-2007
Document Type
Article
Language
English
First Page
2497
Last Page
2516
WOS Identifier
ISSN
1462-5814
Recommended Citation
"The carboxyl-terminal SH3 domain of the mammalian adaptor CrkII promotes internalization of Listeria monocytogenes through activation of host phosphoinositide 3-kinase" (2007). Faculty Bibliography 2000s. 7061.
https://stars.library.ucf.edu/facultybib2000/7061
Comments
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