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Structural insights into interaction between mammalian methionine sulfoxide reductase B1 and thioredoxin. / Dobrovolska, Olena; Rychkov, Georgy; Shumilina, Elena; Nerinovski, Kirill; Schmidt, Alexander; Shabalin, Konstantin; Yakimov, Alexander; Dikiy, Alexander.

в: Journal of Biomedicine and Biotechnology, Том 2012, 586539, 2012.

Результаты исследований: Научные публикации в периодических изданияхстатьяРецензирование

Harvard

Dobrovolska, O, Rychkov, G, Shumilina, E, Nerinovski, K, Schmidt, A, Shabalin, K, Yakimov, A & Dikiy, A 2012, 'Structural insights into interaction between mammalian methionine sulfoxide reductase B1 and thioredoxin', Journal of Biomedicine and Biotechnology, Том. 2012, 586539. https://doi.org/10.1155/2012/586539

APA

Dobrovolska, O., Rychkov, G., Shumilina, E., Nerinovski, K., Schmidt, A., Shabalin, K., Yakimov, A., & Dikiy, A. (2012). Structural insights into interaction between mammalian methionine sulfoxide reductase B1 and thioredoxin. Journal of Biomedicine and Biotechnology, 2012, [586539]. https://doi.org/10.1155/2012/586539

Vancouver

Dobrovolska O, Rychkov G, Shumilina E, Nerinovski K, Schmidt A, Shabalin K и пр. Structural insights into interaction between mammalian methionine sulfoxide reductase B1 and thioredoxin. Journal of Biomedicine and Biotechnology. 2012;2012. 586539. https://doi.org/10.1155/2012/586539

Author

Dobrovolska, Olena ; Rychkov, Georgy ; Shumilina, Elena ; Nerinovski, Kirill ; Schmidt, Alexander ; Shabalin, Konstantin ; Yakimov, Alexander ; Dikiy, Alexander. / Structural insights into interaction between mammalian methionine sulfoxide reductase B1 and thioredoxin. в: Journal of Biomedicine and Biotechnology. 2012 ; Том 2012.

BibTeX

@article{319692c50ac7490d802a697c3393f1d8,
title = "Structural insights into interaction between mammalian methionine sulfoxide reductase B1 and thioredoxin",
abstract = "Maintenance of the cellular redox balance has vital importance for correcting organism functioning. Methionine sulfoxide reductases (Msrs) are among the key members of the cellular antioxidant defence system. To work properly, methionine sulfoxide reductases need to be reduced by their biological partner, thioredoxin (Trx). This process, according to the available kinetic data, represents the slowest step in the Msrs catalytic cycle. In the present paper, we investigated structural aspects of the intermolecular complex formation between mammalian MsrB1 and Trx. NMR spectroscopy and biocomputing were the two mostly used through the research approaches. The formation of NMR detectable MsrB1/Trx complex was monitored and studied in attempt to understand MsrB1 reduction mechanism. Using NMR data, molecular mechanics, protein docking, and molecular dynamics simulations, it was found that intermediate MsrB1/Trx complex is stabilized by interprotein -layer. The complex formation accompanied by distortion of disulfide bond within MsrB1 facilitates the reduction of oxidized MsrB1 as it is evidenced by the obtained data.",
author = "Olena Dobrovolska and Georgy Rychkov and Elena Shumilina and Kirill Nerinovski and Alexander Schmidt and Konstantin Shabalin and Alexander Yakimov and Alexander Dikiy",
note = "Copyright: Copyright 2012 Elsevier B.V., All rights reserved.",
year = "2012",
doi = "10.1155/2012/586539",
language = "English",
volume = "2012",
journal = "BioMed Research International",
issn = "2314-6133",
publisher = "Hindawi ",

}

RIS

TY - JOUR

T1 - Structural insights into interaction between mammalian methionine sulfoxide reductase B1 and thioredoxin

AU - Dobrovolska, Olena

AU - Rychkov, Georgy

AU - Shumilina, Elena

AU - Nerinovski, Kirill

AU - Schmidt, Alexander

AU - Shabalin, Konstantin

AU - Yakimov, Alexander

AU - Dikiy, Alexander

N1 - Copyright: Copyright 2012 Elsevier B.V., All rights reserved.

PY - 2012

Y1 - 2012

N2 - Maintenance of the cellular redox balance has vital importance for correcting organism functioning. Methionine sulfoxide reductases (Msrs) are among the key members of the cellular antioxidant defence system. To work properly, methionine sulfoxide reductases need to be reduced by their biological partner, thioredoxin (Trx). This process, according to the available kinetic data, represents the slowest step in the Msrs catalytic cycle. In the present paper, we investigated structural aspects of the intermolecular complex formation between mammalian MsrB1 and Trx. NMR spectroscopy and biocomputing were the two mostly used through the research approaches. The formation of NMR detectable MsrB1/Trx complex was monitored and studied in attempt to understand MsrB1 reduction mechanism. Using NMR data, molecular mechanics, protein docking, and molecular dynamics simulations, it was found that intermediate MsrB1/Trx complex is stabilized by interprotein -layer. The complex formation accompanied by distortion of disulfide bond within MsrB1 facilitates the reduction of oxidized MsrB1 as it is evidenced by the obtained data.

AB - Maintenance of the cellular redox balance has vital importance for correcting organism functioning. Methionine sulfoxide reductases (Msrs) are among the key members of the cellular antioxidant defence system. To work properly, methionine sulfoxide reductases need to be reduced by their biological partner, thioredoxin (Trx). This process, according to the available kinetic data, represents the slowest step in the Msrs catalytic cycle. In the present paper, we investigated structural aspects of the intermolecular complex formation between mammalian MsrB1 and Trx. NMR spectroscopy and biocomputing were the two mostly used through the research approaches. The formation of NMR detectable MsrB1/Trx complex was monitored and studied in attempt to understand MsrB1 reduction mechanism. Using NMR data, molecular mechanics, protein docking, and molecular dynamics simulations, it was found that intermediate MsrB1/Trx complex is stabilized by interprotein -layer. The complex formation accompanied by distortion of disulfide bond within MsrB1 facilitates the reduction of oxidized MsrB1 as it is evidenced by the obtained data.

UR - http://www.scopus.com/inward/record.url?scp=84859726670&partnerID=8YFLogxK

U2 - 10.1155/2012/586539

DO - 10.1155/2012/586539

M3 - Article

C2 - 22505815

AN - SCOPUS:84859726670

VL - 2012

JO - BioMed Research International

JF - BioMed Research International

SN - 2314-6133

M1 - 586539

ER -

ID: 73950022