scholarly journals SH3-dependent assembly of the phagocyte NADPH oxidase.

1994 ◽  
Vol 180 (6) ◽  
pp. 2011-2015 ◽  
Author(s):  
L C McPhail
Author(s):  
Sylvie Berthier ◽  
Athan Baillet ◽  
Marie-Helene Paclet ◽  
Philippe Gaudin ◽  
Francoise Morel

2020 ◽  
Vol 177 ◽  
pp. 113950
Author(s):  
Coralie Pintard ◽  
Marwa Ben Khemis ◽  
Dan Liu ◽  
Pham My-Chan Dang ◽  
Margarita Hurtado-Nedelec ◽  
...  

Blood ◽  
2014 ◽  
Vol 123 (14) ◽  
pp. 2129-2130
Author(s):  
Richard D. Ye

2016 ◽  
pp. fuw042 ◽  
Author(s):  
Helene Buvelot ◽  
Klara M. Posfay-Barbe ◽  
Patrick Linder ◽  
Jacques Schrenzel ◽  
Karl-Heinz Krause

1995 ◽  
Vol 182 (3) ◽  
pp. 751-758 ◽  
Author(s):  
S H Jackson ◽  
J I Gallin ◽  
S M Holland

Chronic granulomatous disease (CGD) is caused by a congenital defect in phagocyte reduced nicotinamide dinucleotide phosphate (NADPH) oxidase production of superoxide and related species. It is characterized by recurrent life-threatening bacterial and fungal infections and tissue granuloma formation. We have created a mouse model of CGD by targeted disruption of p47phox, one of the genes in which mutations cause human CGD. Identical to the case in human CGD, leukocytes from p47phox-/- mice produced no superoxide and killed staphylococci ineffectively. p47phox-/- mice developed lethal infections and granulomatous inflammation similar to those encountered in human CGD patients. This model mirrors human CGD and confirms a critical role for the phagocyte NADPH oxidase in mammalian host defense.


2018 ◽  
Vol 1859 ◽  
pp. e48
Author(s):  
Xavier Serfaty ◽  
Pauline Lefrançois ◽  
Chantal Houée-Levin ◽  
Stéphane Arbault ◽  
Laura Baciou ◽  
...  

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