EC Number   |
Protein Variants |
Reference |
|---|
   2.3.2.8 | C315A |
full enzyme activity |
488022 |
| 2.3.2.8 | F313A |
slight decrease in activity |
673339 |
| 2.3.2.8 | K417A |
no detectable enzymatic activity |
673339 |
| 2.3.2.8 | malfunction |
knockout of ATE1 gene in MEFs significantly reduces apoptotic rates in the presence of microbial alkaloid toxin staurosporine (STS) compared to wild-type. Similar results are observed with a different stressor, CdCl2 |
759021 |
| 2.3.2.8 | more |
ATE abundance underlies spatiotemporal patterning in the moss Physcomitrella patens using a translational GUS reporter fusion via knock-in at the endogenous genomic locus. The tagged version of ATE is used to pull down specifically ATE together with potential interaction partners from tissues where ATE abundance is monitored via histochemical GUS staining |
759770 |
| 2.3.2.8 | more |
construction of a conditional mouse ATE1 knockout model (Ate1-floxed mice), phenotype, overview. Complete Ate1 knockout mice die at E12.5-E14.5 during development. Nes-Ate1 mice develope to full term and are born at the expected about 25% ratio, with the body weight and appearance at birth indistinguishable from their wild-type littermates. However, these newborn mice are visibly less active than wild-type, easily pushed away by their littermates during feeding and show no inclination to explore the environment within days after birth. These newborns exhibit dramatically reduced growth in the first days of postnatal life, likely due to their inability to compete for the mother's milk with wild-type littermates. Brain phenotypes, overview. Lack of arginylation causes defects in neurite outgrowth |
759108 |
| 2.3.2.8 | more |
for the generation of ATE1 knockdown hypertrophied rats, ATE1 siRNA is encapsulated in stearic acid-modified carboxy methyl chitosan (CMC) conjugated to a cardiomyocyte-targeting peptide. Cardiac function is improved in terms of left ventricular diastolic dysfunction (LVDd) and fractional shortening (%FS) in the ligated + ATE1-siRNA as compared to the Ligated + NS-siRNA when examined by M-Mode echocardiography. Cardiac ATE1 deficiency restores cardiac dysfunction after right renal artery ligation. ATE1 knockdown H9C2 cells |
760135 |
| 2.3.2.8 | more |
generation of ate1 knockout fibroblasts |
759021 |
| 2.3.2.8 | more |
generation of Ate1 knockout mice and Ate1 knockout mouse embryonic fibroblasts, phenotypes, overview. alpha-Syn-transfected Ate1 knockout cells are treated with chloroquine and bafilomycin, the inhibitors of lysosomal degradation and autophagy previously shown to interfere with alpha-syn removal from normal cells. Neither of these treatments in Ate1 knockout leads to the expected increase in intracellular levels of alpha-syn, suggesting that neither lysosomal degradation nor autophagy contribute substantially to the removal of alpha-syn, in the absence of arginylation |
760145 |
| 2.3.2.8 | more |
generation of ATE1-/- deletion mice. Genotyping of litter embryos at E14.5 retrieved from the ATE+/- intercross reveals no live homozygous mutants, indicating that the deletion of the ATE1 gene is lethal at midgestation. Defective neuronal-cell proliferation in the ATE1-null embryonic brain, overview |
-, 758964 |
