Correction to: Exploring the biological functional mechanism of the HMGB1/TLR4/MD-2 complex by surface plasmon resonance

被引:0
|
作者
Mingzhu He
Marco E. Bianchi
Tom R. Coleman
Kevin J. Tracey
Yousef Al-Abed
机构
[1] Center for Molecular Innovation,Division of Genetics and Cell Biology, Chromatin Dynamics Unit
[2] The Feinstein Institute for Medical Research,undefined
[3] San Raffaele University and San Raffaele Scientific Institute IRCCS,undefined
[4] Center for Biomedical Science,undefined
[5] and Center for Bioelectronic Medicine,undefined
[6] The Feinstein Institute for Medical Research,undefined
来源
Molecular Medicine | 2018年 / 24卷
关键词
D O I
暂无
中图分类号
学科分类号
摘要
After publication of this article (He et al., 2018), the corresponding authors recognised an error in Scheme 1, in particular to section “A. HMGB1/TLR4/MD-2 complex formation”. Above “Step 2: B box binding to MD-2”, the text incorrectly read: “Low affinity / extremely slow off”. In addition, some text was omitted below “TLR4/MD-2”. The correct version of Scheme 1 is included in this Correction article. The original article (He et al., 2018) has been corrected.
引用
收藏
相关论文
共 50 条
  • [31] MD-2 expression is not required for cell surface targeting of Toll-like receptor 4 (TLR4)
    Visintin, Alberto
    Halmen, Kristen A.
    Khan, Naseema
    Monks, Brian G.
    Golenbock, Douglas T.
    Lien, Egil
    JOURNAL OF LEUKOCYTE BIOLOGY, 2006, 80 (06) : 1584 - 1592
  • [32] A designed TLR4/MD-2 complex to capture LPS (vol 11, pg 197, 2005)
    Brandl, Katharina
    Glueck, Thomas
    Hartmann, Pia
    Salzberger, Bernd
    Falk, Werner
    INNATE IMMUNITY, 2012, 18 (04) : 672 - 672
  • [33] Proinflammatory cytokine HMGB1 increases leptin secretion with a TLR2/TLR4 mechanism in type 2 diabetes related inflammation
    Coppola, A.
    Capuani, B.
    Pacifici, F.
    Pastore, D.
    Arriga, R.
    Rea, S.
    Andreadi, A.
    Bellia, A.
    Tesauro, M.
    Della-Morte, D.
    Sconocchia, G.
    Lauro, D.
    DIABETOLOGIA, 2019, 62 : S316 - S316
  • [34] The lipopolysaccharide-recognition mechanism in cells expressing TLR4 and CD14 but lacking MD-2
    Ohnishi, Takahiro
    Muroi, Masashi
    Tanamoto, Ken-ichi
    FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY, 2007, 51 (01): : 84 - 91
  • [35] Correlation of HMGB1, TLR2 and TLR4 with left ventricular diastolic dysfunction in sepsis patients
    Lv, Xinwei
    Shi, Xiaohui
    Maihemuti, Mutalifu
    Yang, Danping
    Xiao, Dong
    SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 2023, 97 (04)
  • [36] Radioiodination of an endotoxin•MD-2 complex generates a novel sensitive, high-affinity ligand for TLR4
    Teghanemt, Athmane
    Weiss, Jerrold P.
    Gioannini, Theresa L.
    INNATE IMMUNITY, 2013, 19 (05) : 545 - 560
  • [37] SERUM HMGB1 AND TLR4 LEVELS AS NOVEL BIOLOGICAL MARKERS FOR THE ACTIVITIES OF NEUROPSYCHIATRIC SYSTEMIC LUPUS ERYTHEMATOSUS
    Huang, Q.
    Yuan, C.
    Ren, H.
    Yang, M.
    ANNALS OF THE RHEUMATIC DISEASES, 2017, 76 : 294 - 294
  • [38] TLR4/MD-2 and RP105/MD-1 differentially regulate LPS responsiveness in B cells
    Nagai, Yoshinori
    Ohta, Shoichiro
    Miyake, Kensuke
    Takatsu, Kiyoshi
    JOURNAL OF IMMUNOLOGY, 2009, 182
  • [39] HMGB1 induces chondrocyte hypertrophy and matrix catabolism via TLR2 and TLR4 signaling in chondrocytes
    Bryan, Ru L.
    Terkeltaub, Robert
    ARTHRITIS AND RHEUMATISM, 2008, 58 (09): : S873 - S874
  • [40] Identification of mouse MD-2 residues important for forming the cell surface TLR4-MD-2 complex recognized by anti-TLR4-MD-2 antibodies, and for conferring LPS and taxol responsiveness on mouse TLR4 by alanine-scanning mutagenesis
    Kawasaki, K
    Nogawa, H
    Nishijima, M
    JOURNAL OF IMMUNOLOGY, 2003, 170 (01): : 413 - 420