EC Number   |
General Information |
Reference |
|---|
   2.3.2.8 | malfunction |
deletion of Ate1 in mice leads to embryonic lethality and impairments in multiple physiological systems, including cardiovascular development, angiogenesis, muscle contraction, and cell migration. Lack of arginylation leads to increased Alpha synuclein (alpha-syn) aggregation and causes the formation of larger pathological aggregates in neurons, accompanied by impairments in its ability to be cleared via normal degradation pathways. In the mouse brain, lack of arginylation leads to an increase in alpha-syn's insoluble fraction, accompanied by behavioral changes characteristic for neurodegenerative pathology. Lack of arginylation in the brain leads to neurodegeneration |
760145 |
| 2.3.2.8 | malfunction |
deletion or downregulation of the ATE1 gene disrupts typical stress responses by bypassing growth arrest and suppressing cell death events in the presence of disease-related stressing factors, including oxidative, heat, and osmotic stresses, as well as the exposure to heavy metals or radiation. Conversely, in wild-type cells responding to stress, there is an increase of cellular Ate1 protein level and arginylation activity. The faster growth rates of ate1DELTA mutant yeast in stressing condition compared to wild-type is likely caused by a lack of growth arrest |
-, 759021 |
| 2.3.2.8 | malfunction |
diaphragm myofibrils from enzyme-knockout mice produce an increased force compared to myofibrils from wild type |
736259 |
| 2.3.2.8 | malfunction |
impairments of arginyltransferase ATE1 are implicated in congenital heart defects, obesity, cancer, and neurodegeneration |
718803 |
| 2.3.2.8 | malfunction |
knockdown of arginyltransferase ATE1 attenuates cardiac hypertrophy and fibrosis in vitro and in vivo through the TAK1-JNK1/2 pathway. The cardioprotective role of ATE1 silencing is mediated by the interruption of TAK1 activity-dependent JNK1/2 signaling pathway. The MAPK signaling cascade is one of the signaling pathways involved in cardiac hypertrophy. ATE1 knockdown in presence of cardiac stress performs a cardioprotective action. Cardiac ATE1 deficiency restores cardiac dysfunction after right renal artery ligation. Phenotype, overview |
760135 |
| 2.3.2.8 | malfunction |
knockdown of ATE1 does not significantly influence the mRNA expression of unfolded protein response (UPR) proteins, BiP, CHOP, and ATF4 |
760187 |
| 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 | malfunction |
RAP2.12 stabilization in ate1 ate2 double-null mutant plant lines implicates ATE1 as an ERF-VII-targeting arginyl transferase in vivo |
759833 |
| 2.3.2.8 | malfunction |
the relative abundance of methylesterase 10 (MES10), nucleoside diphosphate kinase family protein (NDPK1), and two asparagine synthetases (ASNs) is augmented in ate1/ate2 mutants. Disrupted ATE1 in dls1 mutants shows an extremely slow age-dependent, dark-induced leaf senescence, phenotype. Double mutant for AtATE1 and AtATE2 (ate1.ate2) displays lost sensitivity to hormone abscisic acid and consequently uncontrolled seed germination and establishment. Arabidopsis ate1/ate2 or prt6 mutants cannot degrade ERFVII, and as a consequence show increased expression of hypoxia-responsive genes involved in fermentation and sugar consumption even under oxygen-rich conditions |
759302 |
| 2.3.2.8 | metabolism |
link between Ate1 and a variety of diseases including cancer |
-, 759021 |
