大葉大學圖書館 |

Gamma-interferon Inducible Lysosomal Thiol Reductase, Its Secretion and Role in Bacterial Infection.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Gamma-interferon Inducible Lysosomal Thiol Reductase, Its Secretion and Role in Bacterial Infection.
Author:	Shuang, Shao.
Description:	115 p.
Notes:	Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.
Contained By:	Dissertation Abstracts International76-11B(E).
Subject:	Biology.
ISBN:	9781321963120
[NT 15000229]:	Gamma-interferon inducible lysosomal thiol reductase (GILT) is a unique thioredoxin that reduces disulfide bonds at acidic pH. GILT can be found in the lysosome in its mature form or secreted as a precursor, both of which are active enzymes. Precursor GILT is constitutively secreted into the murine peritoneal extracellular space. Along with the fully glycosylated precursor, multiple underglycosylated GILT precursors are detected in mouse peritoneal fluid and human ascites, indicating an extracellular mechanism of differential deglycosylation in the peritoneal environment. Bacterial infection induces a time-dependent surge in the peritoneal extracellular GILT levels, which, based on in vitro experiments, is largely contributed by peritoneal macrophages. These findings suggest an extracellular role for GILT both in physiological processes and during inflammation. GILT-deficient peritoneal macrophages produce less reactive oxygen species (ROS) in response to bacterial infection, and exhibit delayed bacterial clearance during the early phase of infection. NADPH oxidase inhibitor treatment negates the difference in bacteria-induced ROS generation, suggesting that GILT regulates NADPH oxidase-dependent ROS production. A proteomics screen has uncovered interesting GILT substrates, offering insights into the potential mechanism for GILT on phagosomal ROS production, as well as its function in the extracellular space.
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3663664

Gamma-interferon Inducible Lysosomal Thiol Reductase, Its Secretion and Role in Bacterial Infection.
Shuang, Shao.

Gamma-interferon Inducible Lysosomal Thiol Reductase, Its Secretion and Role in Bacterial Infection. - 115 p.

Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.

Thesis (Ph.D.)--Yale University, 2015.

Gamma-interferon inducible lysosomal thiol reductase (GILT) is a unique thioredoxin that reduces disulfide bonds at acidic pH. GILT can be found in the lysosome in its mature form or secreted as a precursor, both of which are active enzymes. Precursor GILT is constitutively secreted into the murine peritoneal extracellular space. Along with the fully glycosylated precursor, multiple underglycosylated GILT precursors are detected in mouse peritoneal fluid and human ascites, indicating an extracellular mechanism of differential deglycosylation in the peritoneal environment. Bacterial infection induces a time-dependent surge in the peritoneal extracellular GILT levels, which, based on in vitro experiments, is largely contributed by peritoneal macrophages. These findings suggest an extracellular role for GILT both in physiological processes and during inflammation. GILT-deficient peritoneal macrophages produce less reactive oxygen species (ROS) in response to bacterial infection, and exhibit delayed bacterial clearance during the early phase of infection. NADPH oxidase inhibitor treatment negates the difference in bacteria-induced ROS generation, suggesting that GILT regulates NADPH oxidase-dependent ROS production. A proteomics screen has uncovered interesting GILT substrates, offering insights into the potential mechanism for GILT on phagosomal ROS production, as well as its function in the extracellular space.

ISBN: 9781321963120Subjects--Topical Terms:

171887
Biology.

Gamma-interferon Inducible Lysosomal Thiol Reductase, Its Secretion and Role in Bacterial Infection.
LDR:02300nam a2200265 4500 001 440953
005 20160422125036.5
008 160525s2015 ||||||||||||||||| ||eng d
020 $a 9781321963120
035 $a (MiAaPQ)AAI3663664
035 $a AAI3663664
040 $a MiAaPQ $c MiAaPQ
100 1 $a Shuang, Shao. $3 629971
245 1 0 $a Gamma-interferon Inducible Lysosomal Thiol Reductase, Its Secretion and Role in Bacterial Infection.
300 $a 115 p.
500 $a Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.
500 $a Adviser: Peter Cresswell.
502 $a Thesis (Ph.D.)--Yale University, 2015.
520 $a Gamma-interferon inducible lysosomal thiol reductase (GILT) is a unique thioredoxin that reduces disulfide bonds at acidic pH. GILT can be found in the lysosome in its mature form or secreted as a precursor, both of which are active enzymes. Precursor GILT is constitutively secreted into the murine peritoneal extracellular space. Along with the fully glycosylated precursor, multiple underglycosylated GILT precursors are detected in mouse peritoneal fluid and human ascites, indicating an extracellular mechanism of differential deglycosylation in the peritoneal environment. Bacterial infection induces a time-dependent surge in the peritoneal extracellular GILT levels, which, based on in vitro experiments, is largely contributed by peritoneal macrophages. These findings suggest an extracellular role for GILT both in physiological processes and during inflammation. GILT-deficient peritoneal macrophages produce less reactive oxygen species (ROS) in response to bacterial infection, and exhibit delayed bacterial clearance during the early phase of infection. NADPH oxidase inhibitor treatment negates the difference in bacteria-induced ROS generation, suggesting that GILT regulates NADPH oxidase-dependent ROS production. A proteomics screen has uncovered interesting GILT substrates, offering insights into the potential mechanism for GILT on phagosomal ROS production, as well as its function in the extracellular space.
590 $a School code: 0265.
650 4 $a Biology. $3 171887
690 $a 0306
710 2 $a Yale University. $t Reports on the course of instruction in Yale college. $3 374489
773 0 $t Dissertation Abstracts International $g 76-11B(E).
790 $a 0265
791 $a Ph.D.
792 $a 2015
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3663664