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Dysfonctionnement de la NADPH oxydase des phagocytes dans la granulomatose septique chronique de type X+ Modèle d'étude : les cellules PLB-985 CGD X

Abstract : Mutagenesis approach and stable transfection in the X-CGD PLB-985 cellular model was applied to study the molecular mechanisms of oxidase dysfunction in three X+-CGD cases (H303N/P304R, D500G, L505R), one X–-CGD case (S193F) and the role of two potential cytosolic domains of Nox2 (191TSSTKTIRRS200 and 484DESQANHFAVHHDEEKD500). H303N, P304R and D500G inhibit the assembly and the activity of the oxidase complex. L505R mutation partially diminished the affinity of Nox2 for NADPH and p67phox in a cell-free system assay, but is not involved in the adenine of NADPH binding. The two studied regions are essential to maintain oxidase activity, while only residues 484-500 are associated with the oxidase assembly and electron transfer from NADPH to FAD. The D-loop of Nox1/3/4 is functional for Nox2. The 3D-model of the Nox2 C-terminal confirms that the importance of the alpha-helix loop (484-504) in the oxidase activation.
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https://tel.archives-ouvertes.fr/tel-00010978
Contributor : Xing Jun Li <>
Submitted on : Wednesday, December 28, 2005 - 2:32:33 AM
Last modification on : Friday, November 6, 2020 - 3:59:19 AM
Long-term archiving on: : Tuesday, June 15, 2010 - 4:18:59 PM

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  • HAL Id : tel-00010978, version 1

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Xing Jun Li. Dysfonctionnement de la NADPH oxydase des phagocytes dans la granulomatose septique chronique de type X+ Modèle d'étude : les cellules PLB-985 CGD X. Sciences du Vivant [q-bio]. Université Joseph-Fourier - Grenoble I, 2005. Français. ⟨tel-00010978⟩

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