論文

査読有り
2017年9月

Evaluation of irreversible protein thermal inactivation caused by breakage of disulphide bonds using methanethiosulphonate

SCIENTIFIC REPORTS
  • Junichiro Futami
  • ,
  • Ai Miyamoto
  • ,
  • Atsushi Hagimoto
  • ,
  • Shigeyuki Suzuki
  • ,
  • Midori Futami
  • ,
  • Hiroko Tada

7
1
開始ページ
12471
終了ページ
3275
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41598-017-12748-y
出版者・発行元
NATURE PUBLISHING GROUP

Many extracellular globular proteins have evolved to possess disulphide bonds in their native conformations, which aids in thermodynamic stabilisation. However, disulphide bond breakage by heating leads to irreversible protein denaturation through disulphide-thiol exchange reactions. In this study, we demonstrate that methanethiosulphonate (MTS) specifically suppresses the heat-induced disulphide-thiol exchange reaction, thus improving the heat-resistance of proteins. In the presence of MTS, small globular proteins that contain disulphides can spontaneously refold from heat-denatured states, maintaining wild-type disulphide pairing. Because the disulphide-thiol exchange reaction is triggered by the generation of catalytic amounts of perthiol or thiol, rapid and specific perthiol/thiol protection by MTS reagents prevents irreversible denaturation. Combining MTS reagents with another additive that suppresses chemical modifications, glycinamide, further enhanced protein stabilisation. In the presence of these additives, reliable remnant activities were observed even after autoclaving. However, immunoglobulin G and biotin-binding protein, which are both composed of tetrameric quaternary structures, failed to refold from heat-denatured states, presumably due to chaperon requirements. Elucidation of the chemical modifications involved in irreversible thermoinactivation is useful for the development of preservation buffers with optimum constitutions for specific proteins. In addition, the impact of disulphide bond breakage on the thermoinactivation of proteins can be evaluated using MTS reagents.

リンク情報
DOI
https://doi.org/10.1038/s41598-017-12748-y
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28963503
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000412032600037&DestApp=WOS_CPL
ID情報
  • DOI : 10.1038/s41598-017-12748-y
  • ISSN : 2045-2322
  • PubMed ID : 28963503
  • Web of Science ID : WOS:000412032600037

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