› 4j97

X-ray diffraction
2.55Å resolution

Crystal Structure of FGF Receptor 2 (FGFR2) Kinase Domain Harboring the Pathogenic Gain-of-Function K659E Mutation Identified in Endometrial Cancer.

Released:
DOI: 10.2210/pdb4j97/pdb
PDB entry 4j97 coloured by chain, front view.
PDB entry 4j97 coloured by chain, side view.
PDB entry 4j97 coloured by chain, top view.
Source organism: Homo sapiens
Primary publication:
Cracking the molecular origin of intrinsic tyrosine kinase activity through analysis of pathogenic gain-of-function mutations.
Chen H, Huang Z, Dutta K, Blais S, Neubert TA, Li X, Cowburn D, Traaseth NJ, Mohammadi M
Cell Rep 4 376-84 (2013)
PMID: 23871672

Function and Biology Details

Reaction catalysed: 
ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate
Biochemical function:
Biological process:
Cellular component:
  • not assigned
Sequence domains:

Structure analysis Details

Assemblies composition:
monomeric (preferred)
homo dimer
Assembly name:
PDBe Complex ID:
PDB-CPX-149426 (preferred)
Entry contents:
1 distinct polypeptide molecule
Macromolecule:
Fibroblast growth factor receptor 2 Chains: A, B, C, D
Molecule details ›
Chains: A, B, C, D
Length: 324 amino acids
Theoretical weight: 37.11 KDa
Source organism: Homo sapiens
Expression system: Escherichia coli BL21(DE3)
UniProt:
  • Canonical: P21802 (Residues: 458-768; Coverage: 39%)
Gene names: BEK, FGFR2, KGFR, KSAM
Sequence domains: Protein tyrosine and serine/threonine kinase
Structure domains:

Ligands and Environments

2 bound ligands:
Ligand ACP 4 x ACP
Ligand SO4 5 x SO4
No modified residues

Experiments and Validation Details

Entry percentile scores
X-ray source: NSLS BEAMLINE X4A
Spacegroup: P1
Unit cell:
a: 70.584Å b: 70.278Å c: 85.499Å
α: 92.39° β: 112.19° γ: 115.98°
R-values:
R R work R free
0.202 0.2 0.257
Expression system: Escherichia coli BL21(DE3)

Quick links

Citations

2 review citations

Structure, activation and dysregulation of fibroblast growth factor receptor kinases: perspectives for clinical targeting.
Farrell et al. (2018)
1 more

4 mentions without citation

Cracking the molecular origin of intrinsic tyrosine kinase activity through analysis of pathogenic gain-of-function mutations.
Chen et al. (2013)
3 more