› 6h6k

X-ray diffraction
2Å resolution

The structure of the FKR mutant of the archaeal translation initiation factor 2 gamma subunit in complex with GDPCP, obtained in the absence of magnesium salts in the crystallization solution.

Released:
DOI: 10.2210/pdb6h6k/pdb
PDB entry 6h6k coloured by chain, front view.
PDB entry 6h6k coloured by chain, side view.
PDB entry 6h6k coloured by chain, top view.
Source organism: Saccharolobus solfataricus P2
Primary publication:
The third structural switch in the archaeal translation initiation factor 2 (aIF2) molecule and its possible role in the initiation of GTP hydrolysis and the removal of aIF2 from the ribosome.
Nikonov O, Kravchenko O, Nevskaya N, Stolboushkina E, Garber M, Nikonov S
Acta Crystallogr D Struct Biol 75 392-399 (2019)
PMID: 30988256

Function and Biology Details

Reaction catalysed: 
GTP + H(2)O = GDP + phosphate
Biochemical function:
Biological process:
Cellular component:
Sequence domains:

Structure analysis Details

Assembly composition:
monomeric (preferred)
Assembly name:
PDBe Complex ID:
PDB-CPX-189088 (preferred)
Entry contents:
1 distinct polypeptide molecule
Macromolecule:
Translation initiation factor 2 subunit gamma Chains: A, B, C, D, E
Molecule details ›
Chains: A, B, C, D, E
Length: 415 amino acids
Theoretical weight: 45.63 KDa
Source organism: Saccharolobus solfataricus P2
Expression system: Escherichia coli
UniProt:
  • Canonical: Q980A5 (Residues: 1-415; Coverage: 100%)
Gene names: SSO0412, eif2g
Sequence domains:
Structure domains:

Ligands and Environments

3 bound ligands:
Ligand GCP 5 x GCP
Ligand NA 6 x NA
Ligand EDO 4 x EDO
No modified residues

Experiments and Validation Details

Entry percentile scores
X-ray source: BESSY BEAMLINE 14.1
Spacegroup: P1
Unit cell:
a: 76.71Å b: 76.75Å c: 146.79Å
α: 101.463° β: 92.077° γ: 95.974°
R-values:
R R work R free
0.217 0.216 0.248
Expression system: Escherichia coli

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Citations

1 citations in other articles

DAPL1 deficiency in mice impairs antioxidant defenses in the RPE and leads to retinal degeneration with AMD-like features.
Ma et al. (2023)