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Conclusions: Riboflavin and light are effective in reducing O. tsutsugamushi.
2
Three strains of O. tsutsugamushi were isolated and all were identified as Kawasaki type.
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Orientia tsutsugamushi causes scrub typhus, a potentially fatal infection that afflicts 1 million people annually.
4
O. tsutsugamushi also impedes ERAD during this time period.
5
It is caused by infection with any of the multitude of strains of the bacterium Orientia tsutsugamushi.
6
The Golgi is also destabilized in cells infected with O. tsutsugamushi or treated with COPB2 small interfering RNA.
7
PCR primers were developed that amplified ompA DNA from all O. tsutsugamushi strains, but not from negative control bacteria.
8
This study demonstrates that O. tsutsugamushi strain Ikeda Anks also bear F-box motifs that interact with host cell polyubiquitination machinery.
9
Rickettsia tsutsugamushi may form an independent lineage, whereas molecular data allow to regroup serologically defined typhus and spotted fever group rickettsiae.
10
Aligning O. tsutsugamushi, poxviral, and eukaryotic F-box sequences delineated three F-box residues that are highly conserved and likely to be functionally important.
11
This study identifies O. tsutsugamushi Anks as T1SS substrates and indicates that many display a tropism for the host cell secretory pathway.
12
The O. tsutsugamushi genome encodes one of the largest known bacterial Ank repertoires plus T1SS and T4SS components.
13
Here, we show that O. tsutsugamushi invokes the UPR in the first 48 h and benefits from ER stress in an amino acid-dependent manner.
14
O. tsutsugamushi growth is minimal during the first 24 to 48 h of infection but its growth becomes logarithmic thereafter.
15
Sustained inhibition of ERAD using RNA interference results in an O. tsutsugamushi growth defect at 72 h that can be rescued by amino acid supplementation.
16
Herein, we determined that the nucleotide and translated amino acid sequences of outer membrane protein A (OmpA) are highly conserved among 51 O. tsutsugamushi isolates.