4QIB

Oxidation-Mediated Inhibition of the Peptidyl-Prolyl Isomerase Pin1


Experimental Data Snapshot

  • Method: X-RAY DIFFRACTION
  • Resolution: 1.86 Å
  • R-Value Free: 0.185 
  • R-Value Work: 0.153 
  • R-Value Observed: 0.156 

wwPDB Validation   3D Report Full Report


This is version 1.2 of the entry. See complete history


Literature

Peroxide-mediated oxidation and inhibition of the peptidyl-prolyl isomerase Pin1.

Innes, B.T.Sowole, M.A.Gyenis, L.Dubinsky, M.Konermann, L.Litchfield, D.W.Brandl, C.J.Shilton, B.H.

(2015) Biochim Biophys Acta 1852: 905-912

  • DOI: https://doi.org/10.1016/j.bbadis.2014.12.025
  • Primary Citation of Related Structures:  
    4QIB

  • PubMed Abstract: 

    Pin1 is a phosphorylation-dependent peptidyl-prolyl isomerase that plays a critical role in mediating protein conformational changes involved in signaling processes related to cell cycle control. Pin1 has also been implicated as being neuroprotective in aging-related neurodegenerative disorders including Alzheimer's disease where Pin1 activity is diminished. Notably, recent proteomic analysis of brain samples from patients with mild cognitive impairment revealed that Pin1 is oxidized and also displays reduced activity. Since the Pin1 active site contains a functionally critical cysteine residue (Cys113) with a low predicted pK(a), we hypothesized that Cys113 is sensitive to oxidation. Consistent with this hypothesis, we observed that treatment of Pin1 with hydrogen peroxide results in a 32Da mass increase, likely resulting from the oxidation of Cys113 to sulfinic acid (Cys-SO(2)H). This modification results in loss of peptidyl-prolyl isomerase activity. Notably, Pin1 with Cys113 substituted by aspartic acid retains activity and is no longer sensitive to oxidation. Structural studies by X-ray crystallography revealed increased electron density surrounding Cys113 following hydrogen peroxide treatment. At lower concentrations of hydrogen peroxide, oxidative inhibition of Pin1 can be partially reversed by treatment with dithiothreitol, suggesting that oxidation could be a reversible modification with a regulatory role. We conclude that the loss of Pin1 activity upon oxidation results from oxidative modification of the Cys113 sulfhydryl to sulfenic (Cys-SOH) or sulfinic acid (Cys-SO(2)H). Given the involvement of Pin1 in pathological processes related to neurodegenerative diseases and to cancer, these findings could have implications for the prevention or treatment of disease.


  • Organizational Affiliation

    Department of Biochemistry, Schulich School of Medicine and Dentistry, The University of Western Ontario, Canada.


Macromolecules
Find similar proteins by:  (by identity cutoff)  |  3D Structure
Entity ID: 1
MoleculeChains Sequence LengthOrganismDetailsImage
Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1159Homo sapiensMutation(s): 1 
Gene Names: PIN1
EC: 5.2.1.8
UniProt & NIH Common Fund Data Resources
Find proteins for Q13526 (Homo sapiens)
Explore Q13526 
Go to UniProtKB:  Q13526
PHAROS:  Q13526
GTEx:  ENSG00000127445 
Entity Groups  
Sequence Clusters30% Identity50% Identity70% Identity90% Identity95% Identity100% Identity
UniProt GroupQ13526
Sequence Annotations
Expand
  • Reference Sequence
Experimental Data & Validation

Experimental Data

  • Method: X-RAY DIFFRACTION
  • Resolution: 1.86 Å
  • R-Value Free: 0.185 
  • R-Value Work: 0.153 
  • R-Value Observed: 0.156 
  • Space Group: P 31 2 1
Unit Cell:
Length ( Å )Angle ( ˚ )
a = 68.53α = 90
b = 68.53β = 90
c = 79.27γ = 120
Software Package:
Software NamePurpose
MAR345dtbdata collection
PHENIXmodel building
PHENIXrefinement
MOSFLMdata reduction
SCALAdata scaling
PHENIXphasing

Structure Validation

View Full Validation Report



Entry History 

Deposition Data

Revision History  (Full details and data files)

  • Version 1.0: 2015-02-04
    Type: Initial release
  • Version 1.1: 2015-03-04
    Changes: Database references
  • Version 1.2: 2024-11-27
    Changes: Data collection, Database references, Derived calculations, Structure summary