PLoS Pathog 2014 Jul 31;10(7):e1004295. Epub 2014 Jul 31.
Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, United States of America; California NanoSystems Institute, University of California, Los Angeles, Los Angeles, California, United States of America.
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J Biol Chem 2013 Mar 10;288(11):7492-505. Epub 2013 Jan 10.
Department of Microbiology, University of Illinois, Urbana, Illinois 61801, USA.
The cytolethal distending toxins (CDTs) compose a subclass of intracellularly acting genotoxins produced by many Gram-negative pathogenic bacteria that disrupt the normal progression of the eukaryotic cell cycle. Here, the intoxication mechanisms of CDTs from Escherichia coli (Ec-CDT) and Haemophilus ducreyi (Hd-CDT), which share limited amino acid sequence homology, were directly compared. Ec-CDT and Hd-CDT shared comparable in vitro DNase activities of the CdtB subunits, saturable cell surface binding with comparable affinities, and the requirement for an intact Golgi complex to induce cell cycle arrest. Read More
J Biol Chem 2010 Jun 12;285(24):18199-207. Epub 2010 Apr 12.
Department of Microbiology, University of California, Los Angeles, California 90095, USA.
Cytolethal distending toxins (CDTs) are tripartite protein exotoxins produced by a diverse group of pathogenic Gram-negative bacteria. Based on their ability to induce DNA damage, cell cycle arrest, and apoptosis of cultured cells, CDTs are proposed to enhance virulence by blocking cellular division and/or directly killing epithelial and immune cells. Despite the widespread distribution of CDTs among several important human pathogens, our understanding of how these toxins interact with host cells is limited. Read More
Cell Microbiol 2005 Jul;7(7):921-34
Microbiology and Tumorbiology Center, Karolinska Institutet, Stockholm, Sweden.
The cytolethal distending toxins (CDTs) are unique in their ability to induce DNA damage, activate checkpoint responses and cause cell cycle arrest or apoptosis in intoxicated cells. However, little is known about their cellular internalization pathway. We demonstrate that binding of the Haemophilus ducreyi CDT (HdCDT) on the plasma membrane of sensitive cells was abolished by cholesterol extraction with methyl-beta-cyclodextrin. Read More
MBio 2017 03 28;8(2). Epub 2017 Mar 28.
Department of Molecular Biosciences, The University of Texas at Austin, Austin, Texas, USA
Multiple pathogens, including viruses and bacteria, manipulate endoplasmic reticulum-associated degradation (ERAD) to avoid the host immune response and promote their replication. The betaretrovirus mouse mammary tumor virus (MMTV) encodes Rem, which is a precursor protein that is cleaved into a 98-amino-acid signal peptide (SP) and a C-terminal protein (Rem-CT). SP uses retrotranslocation for ER membrane extraction and yet avoids ERAD by an unknown mechanism to enter the nucleus and function as a Rev-like protein. Read More