Small molecule inhibitors of the annexin A2 heterotetramer prevent human papillomavirus type 16 infection
Author(s) -
Andrew W. Woodham,
Julia R. Taylor,
Andrew I. Jimenez,
Joseph G. Skeate,
Thomas Schmidt,
Heike E. Brand,
Diane M. Da Silva,
W. Martin Kast
Publication year - 2015
Publication title -
journal of antimicrobial chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.124
H-Index - 194
eISSN - 1460-2091
pISSN - 0305-7453
DOI - 10.1093/jac/dkv045
Subject(s) - heterotetramer , annexin a2 , biology , cytotoxicity , trypan blue , hela , annexin , microbiology and biotechnology , flow cytometry , in vitro , immunology , biochemistry , protein subunit , gene
High-risk human papillomavirus (HPV) infection leads to the development of several human cancers that cause significant morbidity and mortality worldwide. HPV type 16 (HPV16) is the most common of the cancer-causing genotypes and gains entry to the basal cells of the epithelium through a non-canonical endocytic pathway that involves the annexin A2/S100A10 heterotetramer (A2t). A2t is composed of two annexin A2 monomers bound to an S100A10 dimer and this interaction is a potential target to block HPV16 infection. Here, recently identified small molecule inhibitors of A2t (A2ti) were investigated for their ability to prevent HPV16 infection in vitro.
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