Subject: | |
From: | |
Reply To: | |
Date: | Thu, 19 Apr 2012 12:08:02 -0400 |
Content-Type: | multipart/alternative |
Parts/Attachments: |
|
|
> Thesis Defense Announcement
> To: The George Mason University Community
>
> *Candidate: Sarah Hamer
> Program: Master of Science in Biology
> *
> *Date: Wednesday April 25, 2012
> Time: 10:00 a.m.
> Place: George Mason University, Prince William campus <http://www.gmu.edu/resources/visitors/findex.html>
> Bull Run Hall, Room 247
>
> *Thesis Chair: Dr. Serguei Popov
> Thesis Director: Dr. Myung-Chul Chung
>
> Title: "The S-nitrosylation of Peroxiredoxin 1 in Human Small Airway Epithelial Cells During Bacillus Anthracis Infection"
> A copy of the thesis is on reserve in the Johnson Center Library,
> Fairfax campus. The thesis will not be read at the meeting, but
> should be read in advance. All members of the George Mason University
> community are invited to attend.
>
> *ABSTRACT:
> *Bacillus anthracis, a Gram-positive soil organism, is the causative
> agent of anthrax. Although the key virulence factor of anthrax is
> mediated by toxins (i.e. lethal toxin and edema toxin), it has proven
> that the bacterial nitric oxide synthase (bNOS) of B. anthracis, also,
> plays a role in pathogenesis. Since B. anthracis infection produced
> bona fide nitric oxide that is responsible for protein modification by
> S-nitrosylation, I hypothesized that bNOS-induced nitric oxide
> contributes to regulation of host cell function through protein
> chemical modification. The nitrosproteomic analysis using the
> biotin-switch assay demonstrated that during B. anthracis infection,
> peroxiredoxin 1 (Prx1) was predominantly S-nitrosylated; there was a
> decrease in its peroxidase activity and an increase in its chaperone
> activity, which both affect cell viability. Treatment with a nitric
> oxide donor in a high hydrogen peroxide environment decreased cell
> viability; while during B. anthracis there was an increase in cell
> viability, presumably due to increase of chaperone activity of Prx1.
> These results suggest that during B. anthracis infection,
> bacteria-derived nitric oxide plays a role in oxidative or nitrosative
> stress-induced epithelial responses to the pathogen in the lung.
>
> //
> ###**
>
>
|
|
|