3S9O

The Focal Adhesion Targeting (FAT) domain of the Focal Adhesion Kinase showing N-terminal interactions in cis


Experimental Data Snapshot

  • Method: X-RAY DIFFRACTION
  • Resolution: 2.60 Å
  • R-Value Free: 0.287 
  • R-Value Work: 0.233 
  • R-Value Observed: 0.234 

wwPDB Validation   3D Report Full Report


This is version 1.2 of the entry. See complete history


Literature

Conformational dynamics of the focal adhesion targeting domain control specific functions of focal adhesion kinase in cells.

Kadare, G.Gervasi, N.Brami-Cherrier, K.Blockus, H.El Messari, S.Arold, S.T.Girault, J.A.

(2015) J Biol Chem 290: 478-491

  • DOI: https://doi.org/10.1074/jbc.M114.593632
  • Primary Citation of Related Structures:  
    3S9O

  • PubMed Abstract: 

    Focal adhesion (FA) kinase (FAK) regulates cell survival and motility by transducing signals from membrane receptors. The C-terminal FA targeting (FAT) domain of FAK fulfils multiple functions, including recruitment to FAs through paxillin binding. Phosphorylation of FAT on Tyr(925) facilitates FA disassembly and connects to the MAPK pathway through Grb2 association, but requires dissociation of the first helix (H1) of the four-helix bundle of FAT. We investigated the importance of H1 opening in cells by comparing the properties of FAK molecules containing wild-type or mutated FAT with impaired or facilitated H1 openings. These mutations did not alter the activation of FAK, but selectively affected its cellular functions, including self-association, Tyr(925) phosphorylation, paxillin binding, and FA targeting and turnover. Phosphorylation of Tyr(861), located between the kinase and FAT domains, was also enhanced by the mutation that opened the FAT bundle. Similarly phosphorylation of Ser(910) by ERK in response to bombesin was increased by FAT opening. Although FAK molecules with the mutation favoring FAT opening were poorly recruited at FAs, they efficiently restored FA turnover and cell shape in FAK-deficient cells. In contrast, the mutation preventing H1 opening markedly impaired FAK function. Our data support the biological importance of conformational dynamics of the FAT domain and its functional interactions with other parts of the molecule.


  • Organizational Affiliation

    From the INSERM, UMR-S 839, F-75005 Paris, France, the Université Pierre & Marie Curie (UPMC), Sorbonne Universités, F-75005 Paris, France, the Institut du Fer à Moulin, F-75005 Paris, France.


Macromolecules
Find similar proteins by:  (by identity cutoff)  |  3D Structure
Entity ID: 1
MoleculeChains Sequence LengthOrganismDetailsImage
Focal adhesion kinase 1
A, B, C
164Homo sapiensMutation(s): 0 
Gene Names: FAKFAK1PTK2
EC: 2.7.10.2
UniProt & NIH Common Fund Data Resources
Find proteins for Q05397 (Homo sapiens)
Explore Q05397 
Go to UniProtKB:  Q05397
PHAROS:  Q05397
GTEx:  ENSG00000169398 
Entity Groups  
Sequence Clusters30% Identity50% Identity70% Identity90% Identity95% Identity100% Identity
UniProt GroupQ05397
Sequence Annotations
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  • Reference Sequence
Experimental Data & Validation

Experimental Data

  • Method: X-RAY DIFFRACTION
  • Resolution: 2.60 Å
  • R-Value Free: 0.287 
  • R-Value Work: 0.233 
  • R-Value Observed: 0.234 
  • Space Group: C 2 2 21
Unit Cell:
Length ( Å )Angle ( ˚ )
a = 89.918α = 90
b = 223.983β = 90
c = 98.015γ = 90
Software Package:
Software NamePurpose
ADSCdata collection
MOLREPphasing
REFMACrefinement
MOSFLMdata reduction
SCALAdata scaling

Structure Validation

View Full Validation Report



Entry History 

Deposition Data

  • Released Date: 2012-06-06 
  • Deposition Author(s): Arold, S.T.

Revision History  (Full details and data files)

  • Version 1.0: 2012-06-06
    Type: Initial release
  • Version 1.1: 2015-02-25
    Changes: Database references
  • Version 1.2: 2023-09-13
    Changes: Data collection, Database references, Derived calculations, Refinement description