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7PI6

Trypanosoma brucei ISG65 bound to human complement C3d

7PI6 の概要
エントリーDOI10.2210/pdb7pi6/pdb
分子名称65 kDa invariant surface glycoprotein, Complement C3dg fragment, GLYCEROL, ... (5 entities in total)
機能のキーワードcomplement, innate immunity, host-pathogen, sleeping sickness, immune system
由来する生物種Trypanosoma brucei brucei (strain 927/4 GUTat10.1)
詳細
タンパク質・核酸の鎖数4
化学式量合計154743.35
構造登録者
Cook, A.D.,Higgins, M.K. (登録日: 2021-08-19, 公開日: 2022-07-27, 最終更新日: 2024-10-16)
主引用文献Macleod, O.J.S.,Cook, A.D.,Webb, H.,Crow, M.,Burns, R.,Redpath, M.,Seisenberger, S.,Trevor, C.E.,Peacock, L.,Schwede, A.,Kimblin, N.,Francisco, A.F.,Pepperl, J.,Rust, S.,Voorheis, P.,Gibson, W.,Taylor, M.C.,Higgins, M.K.,Carrington, M.
Invariant surface glycoprotein 65 of Trypanosoma brucei is a complement C3 receptor.
Nat Commun, 13:5085-5085, 2022
Cited by
PubMed Abstract: African trypanosomes are extracellular pathogens of mammals and are exposed to the adaptive and innate immune systems. Trypanosomes evade the adaptive immune response through antigenic variation, but little is known about how they interact with components of the innate immune response, including complement. Here we demonstrate that an invariant surface glycoprotein, ISG65, is a receptor for complement component 3 (C3). We show how ISG65 binds to the thioester domain of C3b. We also show that C3 contributes to control of trypanosomes during early infection in a mouse model and provide evidence that ISG65 is involved in reducing trypanosome susceptibility to C3-mediated clearance. Deposition of C3b on pathogen surfaces, such as trypanosomes, is a central point in activation of the complement system. In ISG65, trypanosomes have evolved a C3 receptor which diminishes the downstream effects of C3 deposition on the control of infection.
PubMed: 36038546
DOI: 10.1038/s41467-022-32728-9
主引用文献が同じPDBエントリー
実験手法
X-RAY DIFFRACTION (2.6 Å)
構造検証レポート
Validation report summary of 7pi6
検証レポート(詳細版)ダウンロードをダウンロード

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件を2024-10-30に公開中

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