EC Number   |
General Information |
Reference |
|---|
   2.5.1.46 | evolution |
CpDHS is more closely related to apicomplexan and human DHS than to kinetoplast DHS |
739026 |
| 2.5.1.46 | evolution |
homospermidine synthase, HSS, EC 2.5.1.44/45, evolved from the gene encoding deoxyhypusine synthase, DHS, by gene duplication. HSS and deoxyhypusine synthase have also diverged with respect to their regulation |
739292 |
| 2.5.1.46 | malfunction |
a haploid Saccharomyces cerevisiae strain with disruption of the DHS gene is not viable, and can be rescued by a plasmid encoding the wild type DHS. When examined under the microscope, a non-viable DHS-disrupted ascus from a tetrad dissection grows several generations to a colony of 100-200 enlarged cells before growth arrest |
701650 |
| 2.5.1.46 | malfunction |
deoxyhypusine synthase haploinsufficiency attenuates acute cytokine signaling, overview. DHS dysfunction in the setting of diabetes mellitus, overview |
-, 721984 |
| 2.5.1.46 | malfunction |
Dhps+/- mice appear normal and do not show any growth defects or phenotypes. When the heterozygous male and female mice are crossed, no pups are born with the genotype of Dhps-/- homozygous deletion, indicating that DHS is vital for growth and survival |
701650 |
| 2.5.1.46 | malfunction |
DHS enzyme inhibition by N1-guanyl-1,7-diaminoheptane results in a significant decrease in tumor formation in vivo. In patients with esophageal squamous cell carcinoma, overexpression of gene DHPS in ESCC tumors is significantly associated with worse recurrence-free survival, and correlated with distant metastasis. Although the mRNA levels of RhoA in DHPS-knockdown cells do not change, RhoA protein levels significantly decrease compared with control |
739208 |
| 2.5.1.46 | malfunction |
DHSL20 lacks the catalytic lysine residue at residue 344, which is indispensable for the enzymatic reaction and is present in the active center for catalysis, and contains leucine instead |
704694 |
| 2.5.1.46 | malfunction |
early flowering phenotype of dexamethasone-treated siDHS knockout transgenic plants, hypersensitivityof siDHS transgenic plants to osmotic stressors and abscisic acid. The sensitivity of transgenic siDHS plantsto abscisic acid in the absence of the silencing drug dexamethasone probably reflects that the genetic inactivation system is slightly leaky and that minor inactivation of the eIF5A pathway is very sensitive to alterations in abscisic acid homeostasis. Non-silenced siDHS plants display partial growth inhibition under salt treatment. Alterations in root cell expansion and root hair phenotypes caused by DHS silencing, overview |
-, 738306 |
| 2.5.1.46 | malfunction |
gene deletion mutations are attempted via targeted gene replacement. Chromosomal null mutants of DHS34 could only be obtained in the presence of a DHS34-containing episome, indicating that DHS34 is an essential gene |
-, 704694 |
| 2.5.1.46 | malfunction |
importance of imbalances in eIF5A hypusination in Fusarium graminearum: overexpression of gene DHS leads to increased virulence in Triticum aestivum, elevated production of the mycotoxin deoxynivalenol, more infection structures, faster Triticum aestivum tissue invasion in plants and increases vegetatively produced conidia. Overexpression of the enzyme DOHH completely prevents infection structure formation, pathogenicity in Triticum aestivum and Zea mays, leads to overproduction of reactive oxygen species, reduced DON mycotoxin production and increased sexual reproduction. Simultaneous overexpression of both genes restores wild type-like phenotypes, strongly increased hypusinated eIF5A in DOHH overexpression mutant in comparison to wild-type, and the DHS overexpression mutants |
739685 |
