Your browser doesn't support javascript.
loading
Mutagenic analysis in a pure molecular system shows that thioredoxin-interacting protein residue Cys247 is necessary and sufficient for a mixed disulfide formation with thioredoxin.
Fould, Benjamin; Lamamy, Véronique; Guenin, Sophie-Penelope; Ouvry, Christine; Cogé, Francis; Boutin, Jean A; Ferry, Gilles.
Afiliación
  • Fould B; Biotechnologies & Pharmacologie Moléculaire et Cellulaire, Institut de Recherches Servier, 125 Chemin de Ronde, 78290 Croissy-sur-Seine, France.
Protein Sci ; 21(9): 1323-33, 2012 Sep.
Article en En | MEDLINE | ID: mdl-22760822
The human thioredoxin (TRX)-interacting protein is found in multiple subcellular compartments and plays a major role in redox homeostasis, particularly in the context of metabolism (e.g., lipidemia and glycemia) and apoptosis. A molecular approach to the protein's modus operandi is still needed because some aspects of the TRX-interacting protein-mediated regulation of TRX are not clearly understood. To this end, His-tagged TRX-interacting proteins were over-expressed in Escherichia coli. Because the protein is expressed mainly in inclusion bodies, it was denatured in high concentrations of guanidium hydrochloride, centrifuged, and purified by Ni-NTA affinity chromatography. His-TRX-interacting protein was then refolded by dialysis and its restructuring monitored by circular dichroism spectrometry. This preparation resulted in the formation of a covalent complex with recombinant human TRX, demonstrating that association occurs without the intervention of other partner proteins. Multiple cysteine-to-serine mutants of TRX-interacting protein were produced and purified. These mutations were efficient in limiting the formation of disulfide-linked homo-oligomers in an oxidizing environment. The mutants were also used to gain functional insight into the formation of the TRX-interacting protein-TRX complexes. These complexes were able to form in the absence of internal disulfide bridges. A mutant with all but one cysteine changed to serine (Cys ²47) also showed an enhanced capacity to form complexes with TRX demonstrating, in a pure molecular system, that this particular cysteine is likely responsible for the disulfide bridge between TRX-interacting protein and TRX.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tiorredoxinas / Proteínas Portadoras / Disulfuros Límite: Animals / Humans Idioma: En Revista: Protein Sci Asunto de la revista: BIOQUIMICA Año: 2012 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tiorredoxinas / Proteínas Portadoras / Disulfuros Límite: Animals / Humans Idioma: En Revista: Protein Sci Asunto de la revista: BIOQUIMICA Año: 2012 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos