Arginine-specific mono ADP-ribosylation in vitro of antimicrobial peptides by ADP-ribosylating toxins.
Arginine-specific mono ADP-ribosylation in vitro of antimicrobial peptides by ADP-ribosylating toxins.
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通过ADP-核糖基毒素,精氨酸特异性的单ADP-核糖基化抗菌肽的体外。
DOI:
10.1371/journal.pone.0041417
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Balducci E
中科院分区:
文献类型:
--
作者:
Castagnini M;Picchianti M;Talluri E;Biagini M;Del Vecchio M;Di Procolo P;Norais N;Nardi-Dei V;Balducci E
Among the several toxins used by pathogenic bacteria to target eukaryotic host cells, proteins that exert ADP-ribosylation activity represent a large and studied family of dangerous and potentially lethal toxins. These proteins alter cell physiology catalyzing the transfer of the ADP-ribose unit from NAD to cellular proteins involved in key metabolic pathways. In the present study, we tested the capability of four of these toxins, to ADP-ribosylate α- and β- defensins. Cholera toxin (CT) from Vibrio cholerae and heat labile enterotoxin (LT) from Escherichia coli both modified the human α-defensin (HNP-1) and β- defensin-1 (HBD1), as efficiently as the mammalian mono-ADP-ribosyltransferase-1. Pseudomonas aeruginosa exoenzyme S was inactive on both HNP-1 and HBD1. Neisseria meningitidis NarE poorly recognized HNP-1 as a substrate but it was completely inactive on HBD1. On the other hand, HNP-1 strongly influenced NarE inhibiting its transferase activity while enhancing auto-ADP-ribosylation. We conclude that only some arginine-specific ADP-ribosylating toxins recognize defensins as substrates in vitro. Modifications that alter the biological activities of antimicrobial peptides may be relevant for the innate immune response. In particular, ADP-ribosylation of antimicrobial peptides may represent a novel escape mechanism adopted by pathogens to facilitate colonization of host tissues.
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影响因子:
2.9
作者:
CERVANTESLAUREAN, D;MINTER, DE;JACOBSON, MK
通讯作者:
JACOBSON, MK
影响因子:
4.8
作者:
Harder, J;Bartels, J;Schröder, JM
通讯作者:
Schröder, JM
DOI:
10.1073/pnas.0500508102
发表时间:
2005-03-29
影响因子:
11.1
作者:
Kim, C;Gajendran, N;Kaufmann, SHE
通讯作者:
Kaufmann, SHE
影响因子:
29.4
作者:
Giesemann, Torsten;Guttenberg, Gregor;Aktories, Klaus
通讯作者:
Aktories, Klaus
影响因子:
4.8
作者:
Ganesan, AK;Frank, DW;Barbieri, JT
通讯作者:
Barbieri, JT