Abstract:
:The bacterial toxin VacA produced by H. pylori induces large vacuoles in several types of cultured cells such as HeLa cells or gastric cells. To determine the mechanism of vacuolation induced by this toxin we employed several inhibitors of membrane trafficking and endocytosis. The development of vacuolation induced by VacA in HeLa cells were prevented by bafilomycin A1 and low temperature conditions that inhibited vesicle transport or endocytosis. Formation of large vacuoles was also inhibited by an antibody against EGF receptor, which was previously shown to be internalized by endocytosis, but not by an anti-transferrin receptor antibody. Moreover, proteins of 58 and 37 kDa, corresponding to fragments of VacA, were recognized by an anti-H. pylori antibody after immunoprecipitation with anti-EGF receptor of cell extracts from HeLa cells treated with VacA, but not from untreated HeLa cells. We suggest that VacA may enter cells by endocytosis mediated by the EGF receptor. These are the first data indicating that the EGF receptor may be significant in the development of vacuolation caused by VacA.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Seto K,Hayashi-Kuwabara Y,Yoneta T,Suda H,Tamaki Hdoi
10.1016/s0014-5793(98)00788-1subject
Has Abstractpub_date
1998-07-24 00:00:00pages
347-50issue
3eissn
0014-5793issn
1873-3468pii
S0014-5793(98)00788-1journal_volume
431pub_type
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