Also hydrolyses other guanosine 5'-triphosphate derivatives with at least one unsubstituted phosphate group on the 3'-position, but not GTP, ATP or adenosine 5'-triphosphate 3'-diphosphate.
the hydrolytic base is E119, the dual specificity typical for the exopolyphosphatase/guanosine pentaphosphate phosphohydrolase protein family is due to a common active site for guanosine pentaphosphate and polyphosphate hydrolysis, R22 and R267, residing in different domains, are crucial for guanosine pentaphosphate specificity as they interact with the unique 3'-ribose phosphorylation
Also hydrolyses other guanosine 5'-triphosphate derivatives with at least one unsubstituted phosphate group on the 3'-position, but not GTP, ATP or adenosine 5'-triphosphate 3'-diphosphate.
not: GTP, ATP or adenosine 5'-triphosphate,3'-diphosphate, guanosine 5'-diphosphate,3'-diphosphate, guanosine 5'-triphosphate,3'-monophosphate-nucleotide, enzyme is rather nonspecific towards the 3'-OH substitutions of the substrates although a free, unsubstituted phosphate group at the 3'-OH position is essential
not: GTP, ATP or adenosine 5'-triphosphate,3'-diphosphate, guanosine 5'-diphosphate,3'-diphosphate, guanosine 5'-triphosphate,3'-monophosphate-nucleotide, enzyme is rather nonspecific towards the 3'-OH substitutions of the substrates although a free, unsubstituted phosphate group at the 3'-OH position is essential
deletion mutants of exopolyphosphatases Ppx1, and the double knockout mutant Ppx1/Ppx2 show decreased accumulation of ppGpp, an alarmone molecule. The lack of ppx gene products results in defects in motility, biofilm formation, nutrient stress survival, invasion and intracellular survival indicating that maintaining a certain level of polyphosphate is critical for Ppx genes in Campylobacter jejuni pathophysiology. Both Ppx1 and Ppx2 mutants are resistant to human complement-mediated killing. The double mutant mutant is sensitive. The serum susceptibility does not occur in the presence of MgCl2 and EGTA. The chicken serum does not have any effect on the mutants' survival. The observed serum susceptibility is not related to surface capsule and lipooligosaccharide structures
double deletion mutants of exopolyphosphatases Ppx1/Ppx2 show decreased accumulation of ppGpp, an alarmone molecule. The lack of ppx gene products results in defects in motility, biofilm formation, nutrient stress survival, invasion and intracellular survival indicating that maintaining a certain level of polyphosphate is critical for Ppx genes in Campylobacter jejuni pathophysiology. Both Ppx1 and Ppx2 mutants are resistant to human complement-mediated killing. The double mutant mutant is sensitive. The serum susceptibility does not occur in the presence of MgCl2 and EGTA. The chicken serum does not have any effect on the mutants' survival. The observed serum susceptibility is not related to surface capsule and lipooligosaccharide structures
double deletion mutants of exopolyphosphatases Ppx1/Ppx2 show decreased accumulation of ppGpp, an alarmone molecule. The lack of ppx gene products results in defects in motility, biofilm formation, nutrient stress survival, invasion and intracellular survival indicating that maintaining a certain level of polyphosphate is critical for Ppx genes in Campylobacter jejuni pathophysiology. Both Ppx1 and Ppx2 mutants are resistant to human complement-mediated killing. The double mutant mutant is sensitive. The serum susceptibility does not occur in the presence of MgCl2 and EGTA. The chicken serum does not have any effect on the mutants' survival. The observed serum susceptibility is not related to surface capsule and lipooligosaccharide structures
deletion mutants of exopolyphosphatases Ppx1, and the double knockout mutant Ppx1/Ppx2 show decreased accumulation of ppGpp, an alarmone molecule. The lack of ppx gene products results in defects in motility, biofilm formation, nutrient stress survival, invasion and intracellular survival indicating that maintaining a certain level of polyphosphate is critical for Ppx genes in Campylobacter jejuni pathophysiology. Both Ppx1 and Ppx2 mutants are resistant to human complement-mediated killing. The double mutant mutant is sensitive. The serum susceptibility does not occur in the presence of MgCl2 and EGTA. The chicken serum does not have any effect on the mutants' survival. The observed serum susceptibility is not related to surface capsule and lipooligosaccharide structures
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CRYSTALLIZATION (Commentary)
ORGANISM
UNIPROT
LITERATURE
PPX/GPPA Y19N mutant enzyme in complex with guanosine tetraphosphate, hanging-drop vapor diffusion method by mixing 0.002 ml of protein and 0.002 ml of reservoir solution containing 200 mM sodium acetate, pH 6.4, 100 mM 4-morpholineethanesulfonic acid, pH 5.7, and 50% methyl-2,4-pentanediol, X-ray diffraction structure determination and analysis at 2.7 A resolution, modelling
sitting drop vapor diffusion method. Apoenzyme, using 20% (w/v) PEG 3350, 0.2 M ammonium sulfate, and 15 mM malic acid. Enzyme in complex with 5'-guanosine-diphosphate-monothiophosphate or phosphoaminophosphonic acid guanylate ester, using 20% (w/v) PEG 3350 and 0.2 M potassium chloride. Enzyme in complex with guanosine tetraphosphate, using 20% (w/v) PEG 3350, 0.2 M ammonium tartrate, and 15 mM malic acid