Table 2.
Pathogen | Protease | Protease category | p65 cleavage site(s) |
Cleavage verification |
Fate and function of p65 fragment |
Proposed mechanism for NF-κB inhibition |
Reference |
---|---|---|---|---|---|---|---|
EPEC, EHEC | NleC | Zinc Metalloprotease | P10/A11 | recombinant in vitro |
Undetermined | Global | Yen et al. 2011 |
EPEC | NleC | Zinc Metalloprotease | Not characterized | in vitro | Undetermined | Global | Muhlen et al. 2011 |
EPEC | NleC | Zinc Metalloprotease | Not characterized | in vitro | Undetermined | Global | Pearson et al. 2011 |
EPEC | NleC | Zinc Metalloprotease | C38/E39 | recombinant in vitro |
Undetermined | Global | Baruch et al. 2011 |
EPEC, C. rodentium |
NleC | Zinc Metalloprotease | Not characterized |
in vitro, in vivo |
Undetermined | Global | Sham et al. 2011 |
EHEC | NleC | Zinc Metalloprotease | C38/E39 | recombinant | Undetermined | Undetermined | Li et al. 2011; Turco & Sousa 2014 |
EPEC, C. rodentium |
NleC | Zinc Metalloprotease | P10/A11, C38/E39 |
in vitro, in vivo |
N-terminal fragment binds RPS3 |
Amplification | Hodgson et al. 2015 |
Phdp | AIP56 | Zinc Metalloprotease | C39/E40 (fish p65) | recombinant in vitro |
Undetermined | Global | Silva et al. 2015 |
C. trachomatis | CT441 | TSP Protease | F351/T352 | in vitro | p40 product binds to IκBα |
Amplification | Lad et al. 2007a; Lad et al. 2007b |
Leishmania | Gp63 | Metalloprotease | C-terminus | in vitro | p35 fragment binds DNA with p50 |
Amplification | Gregory et al. 2008a |
Poliovirus | 3C | Cysteine Protease | Q480/G481 | in vitro | Undetermined | Global | Neznanov et al. 2005 |
HIV-1 | Caspase-3 (host) |
Cysteine Protease | D97/G98 | recombinant in vitro |
binds p50/IκBα | Amplification | Coiras et al. 2008 |
EPEC, Enteropathogenic E. coli; EHEC, Enterohemorrhagic E. coli; Phdp, Photobacterium damselae piscicida; C. trachomatis, Chlamydia trachomatis; HIV, human immunodeficiency virus type 1; recombinant, purified protein assays; in vitro, cell culture/transfection assays; in vivo, animal studies. Global, general blockade of NF-κB signaling either by cleavage alone or in combination with other virulence factors; Amplification, cleaved fragment functions to further the effect of cleaving p65.