› 4y94

X-ray diffraction
2.4Å resolution

Crystal structure of the PH-TH module of Bruton's tyrosine kinase bound to inositol hexakisphosphate

Released:
DOI: 10.2210/pdb4y94/pdb
PDB entry 4y94 coloured by chain, front view.
PDB entry 4y94 coloured by chain, side view.
PDB entry 4y94 coloured by chain, top view.
Source organism: Bos taurus
Primary publication:
Autoinhibition of Bruton's tyrosine kinase (Btk) and activation by soluble inositol hexakisphosphate.
Wang Q, Vogan EM, Nocka LM, Rosen CE, Zorn JA, Harrison SC, Kuriyan J
Elife 4 (2015)
PMID: 25699547

Function and Biology Details

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

Structure analysis Details

Assembly composition:
monomeric (preferred)
Assembly name:
PDBe Complex ID:
PDB-CPX-174901 (preferred)
Entry contents:
1 distinct polypeptide molecule
Macromolecule:
Tyrosine-protein kinase Chains: A, B, C, D
Molecule details ›
Chains: A, B, C, D
Length: 171 amino acids
Theoretical weight: 20.16 KDa
Source organism: Bos taurus
Expression system: Escherichia coli
UniProt:
  • Canonical: Q3ZC95 (Residues: 1-170; Coverage: 26%)
Gene name: BTK
Sequence domains:
Structure domains: Pleckstrin-homology domain (PH domain)/Phosphotyrosine-binding domain (PTB)

Ligands and Environments

2 bound ligands:
Ligand IHP 6 x IHP
Ligand ZN 4 x ZN
No modified residues

Experiments and Validation Details

Entry percentile scores
X-ray source: ALS BEAMLINE 8.2.2
Spacegroup: P1
Unit cell:
a: 37.203Å b: 64.012Å c: 80.029Å
α: 82.08° β: 88.79° γ: 89.89°
R-values:
R R work R free
0.231 0.229 0.255
Expression system: Escherichia coli

Quick links

Citations

16 review citations

Molecular Mechanisms of Human Disease Mediated by Oncogenic and Primary Immunodeficiency Mutations in Class IA Phosphoinositide 3-Kinases.
Dornan et al. (2018)
15 more

6 mentions without citation

The Src module: an ancient scaffold in the evolution of cytoplasmic tyrosine kinases.
Shah et al. (2018)
5 more