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Cystic fibrosis transmembrane conduc...

Kowalski, Michael Paul.

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Cystic fibrosis transmembrane conductance regulator signaling in epithelial cells in response to Pseudomonas aeruginosa.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Cystic fibrosis transmembrane conductance regulator signaling in epithelial cells in response to Pseudomonas aeruginosa./
Author:	Kowalski, Michael Paul.
Description:	85 p.
Notes:	Source: Dissertation Abstracts International, Volume: 66-11, Section: B, page: 5798.
Contained By:	Dissertation Abstracts International66-11B.
Subject:	Biology, Microbiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3194425
ISBN:	9780542391958

Cystic fibrosis transmembrane conductance regulator signaling in epithelial cells in response to Pseudomonas aeruginosa.
Kowalski, Michael Paul.

Cystic fibrosis transmembrane conductance regulator signaling in epithelial cells in response to Pseudomonas aeruginosa. - 85 p.

Source: Dissertation Abstracts International, Volume: 66-11, Section: B, page: 5798.

Thesis (Ph.D.)--Harvard University, 2005.

Cystic fibrosis (CF), a life-shortening disease caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, is commonly associated with the establishment of a chronic infection with the Gram-negative bacterium Pseudomonas aeruginosa and subsequent pulmonary failure. It has been shown that P. aeruginosa binds to the CFTR protein at the first extracellular loop through interaction with the outer core oligosaccharide portion of the bacterial lipopolysaccharide (LPS), and this interaction is required for bacterial internalization, NF-kappaB activation, and apoptosis, all of which are essential for bacterial clearance. The following thesis advances our knowledge of the lung epithelial cell response to P. aeruginosa. It establishes a requirement for wild type CFTR expression for rapid P. aeruginosa -induced apoptosis and CD95/CD95 ligand induction. It also shows that P. aeruginosa binding of CFTR initiates signaling from lipid rafts, and that these rafts are required for epithelial responses to P. aeruginosa. Finally, it demonstrates a role for the poorly understood major vault protein, as a signaling intermediate required for P. aeruginosa internalization and bacterial clearance from the lung. These data help define the signaling of lung epithelial cells in the innate immune response to P. aeruginosa and the deficiencies of CF cells in this response.

ISBN: 9780542391958Subjects--Topical Terms:

1017734
Biology, Microbiology.

Cystic fibrosis transmembrane conductance regulator signaling in epithelial cells in response to Pseudomonas aeruginosa.
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100 1 $a Kowalski, Michael Paul. $3 1914262
245 1 0 $a Cystic fibrosis transmembrane conductance regulator signaling in epithelial cells in response to Pseudomonas aeruginosa.
300 $a 85 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-11, Section: B, page: 5798.
500 $a Adviser: Gerald B. Pier.
502 $a Thesis (Ph.D.)--Harvard University, 2005.
520 $a Cystic fibrosis (CF), a life-shortening disease caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, is commonly associated with the establishment of a chronic infection with the Gram-negative bacterium Pseudomonas aeruginosa and subsequent pulmonary failure. It has been shown that P. aeruginosa binds to the CFTR protein at the first extracellular loop through interaction with the outer core oligosaccharide portion of the bacterial lipopolysaccharide (LPS), and this interaction is required for bacterial internalization, NF-kappaB activation, and apoptosis, all of which are essential for bacterial clearance. The following thesis advances our knowledge of the lung epithelial cell response to P. aeruginosa. It establishes a requirement for wild type CFTR expression for rapid P. aeruginosa -induced apoptosis and CD95/CD95 ligand induction. It also shows that P. aeruginosa binding of CFTR initiates signaling from lipid rafts, and that these rafts are required for epithelial responses to P. aeruginosa. Finally, it demonstrates a role for the poorly understood major vault protein, as a signaling intermediate required for P. aeruginosa internalization and bacterial clearance from the lung. These data help define the signaling of lung epithelial cells in the innate immune response to P. aeruginosa and the deficiencies of CF cells in this response.
590 $a School code: 0084.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Health Sciences, Pathology. $3 1017854
650 4 $a Biology, Cell. $3 1017686
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710 2 0 $a Harvard University. $3 528741
773 0 $t Dissertation Abstracts International $g 66-11B.
790 1 0 $a Pier, Gerald B., $e advisor
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792 $a 2005
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3194425