2QFF

Crystal structure of Staphylococcal Complement Inhibitor


Experimental Data Snapshot

  • Method: X-RAY DIFFRACTION
  • Resolution: 1.80 Å
  • R-Value Free: 0.226 
  • R-Value Work: 0.201 
  • R-Value Observed: 0.202 

wwPDB Validation   3D Report Full Report


This is version 1.1 of the entry. See complete history


Literature

Staphylococcal complement inhibitor: structure and active sites.

Rooijakkers, S.H.Milder, F.J.Bardoel, B.W.Ruyken, M.van Strijp, J.A.Gros, P.

(2007) J Immunol 179: 2989-2998

  • DOI: https://doi.org/10.4049/jimmunol.179.5.2989
  • Primary Citation of Related Structures:  
    2QFF

  • PubMed Abstract: 

    The pathogenic bacterium Staphylococcus aureus counteracts the host immune defense by excretion of the 85 residue staphylococcal complement inhibitor (SCIN). SCIN inhibits the central complement convertases; thereby, it reduces phagocytosis following opsonization and efficiently blocks all downstream effector functions. In this study, we present the crystal structure of SCIN at 1.8 A resolution and the identification of its active site. Functional characterization of structure based chimeric proteins, consisting of SCIN and the structurally but nonfunctional homologue open reading frame-D, indicate an 18-residue segment (Leu-31-Gly-48) crucial for SCIN activity. In all complement activation pathways, chimeras lacking these SCIN residues completely fail to inhibit production of the potent mediator of inflammation C5a. Inhibition of alternative pathway-mediated opsonization (C3b deposition) and formation of the lytic membrane attack complex (C5b-9 deposition) are strongly reduced for these chimeras as well. For inhibition of the classical/lectin pathway-mediated C3b and C5b-9 deposition, the same residues are critical although additional sites are involved. These chimeras also display reduced capacity to stabilize the C3 convertases of both the alternative and the classical/lectin pathway indicating the stabilizing effect is pivotal for the complement inhibitory activity of SCIN. Because SCIN specifically and efficiently inhibits complement, it has a high potential in anti-inflammatory therapy. Our data are a first step toward the development of a second generation molecule suitable for such therapeutic complement intervention.


  • Organizational Affiliation

    Medical Microbiology, University Medical Center Utrecht, Heidelberglaan 100, Utrecht, The Netherlands. s.h.m.rooijakkers@umcutrecht.nl


Macromolecules
Find similar proteins by:  (by identity cutoff)  |  3D Structure
Entity ID: 1
MoleculeChains Sequence LengthOrganismDetailsImage
Hypothetical protein82Staphylococcus aureus subsp. aureus MRSA252Mutation(s): 0 
Gene Names: YP_041408/SAR2035
UniProt
Find proteins for Q6GFB4 (Staphylococcus aureus (strain MRSA252))
Explore Q6GFB4 
Go to UniProtKB:  Q6GFB4
Entity Groups  
Sequence Clusters30% Identity50% Identity70% Identity90% Identity95% Identity100% Identity
UniProt GroupQ6GFB4
Sequence Annotations
Expand
  • Reference Sequence
Small Molecules
Modified Residues  1 Unique
IDChains TypeFormula2D DiagramParent
MSE
Query on MSE
A
L-PEPTIDE LINKINGC5 H11 N O2 SeMET
Experimental Data & Validation

Experimental Data

  • Method: X-RAY DIFFRACTION
  • Resolution: 1.80 Å
  • R-Value Free: 0.226 
  • R-Value Work: 0.201 
  • R-Value Observed: 0.202 
  • Space Group: P 21 21 21
Unit Cell:
Length ( Å )Angle ( ˚ )
a = 23.017α = 90
b = 42.775β = 90
c = 63.91γ = 90
Software Package:
Software NamePurpose
REFMACrefinement
MOSFLMdata reduction
SCALAdata scaling
SOLVEphasing

Structure Validation

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Entry History 

Deposition Data

Revision History  (Full details and data files)

  • Version 1.0: 2007-09-04
    Type: Initial release
  • Version 1.1: 2011-07-13
    Changes: Advisory, Refinement description, Source and taxonomy, Version format compliance