EC Number   |
General Information |
Reference |
|---|
   6.2.1.45 | evolution |
5 amino acids and 8 bases are different in cDNA and DNA sequences of CrUBE1 between Wuzishatangju and Shatangju, respectively |
733931 |
| 6.2.1.45 | evolution |
MUB inhibition of E1 is conserved between plants and humans |
745858 |
| 6.2.1.45 | evolution |
yeast Ub-activating enzyme E1 is a modular protein, evolved from small prokaryotic proteins, which had specific functions, and in E1 enzyme they form domains that work together as part of a big enzyme |
-, 760825 |
| 6.2.1.45 | malfunction |
a defect in the UBA1 gene results in detrimental effects on cell cycle progression, and deletion of the UBA1 gene is lethal to the organism |
-, 760825 |
| 6.2.1.45 | malfunction |
defects in E1 cause apoptotic death of TS-20 cells |
715718 |
| 6.2.1.45 | malfunction |
identification of loss-of-function mutations in the Drosophila ubiquitin activating enzyme, the most upstream enzyme in the ubiquitin pathway. Loss of only one functional copy of E1 caused a significant reduction in adult lifespan. Rare homozygous hypomorphic E1 mutants reach adulthood, but mutants exhibit further reduced lifespan and show inappropriate Ras activation in the brain. Removing just one functional copy of Ras restores the lifespan of heterozygous E1 mutants to that of wild-type flies and increase the survival of homozygous E1 mutants. E1 homozygous mutants also show severe motor impairment involved in early mortality. Phenotypes, detailed overview |
735079 |
| 6.2.1.45 | malfunction |
lethality of RNA antisense silencing of Giardia E1 |
-, 733043 |
| 6.2.1.45 | malfunction |
local delivery of potent chemical UBA1 inhibitor PYR-41 and UBA1 shRNA lentivirus both result in a substantial decrease in intimal hyperplasia at 2 weeks and 4 weeks after balloon injury. UBA1 inhibition also reduces Ki-67 positive cell percentage and inflammatory response in the carotid artery wall. In vitro UBA1 inhibition is able to ameliorate TNF-alpha-induced nuclear factor-kappa B (NF-kappaB) activation by reducing IkappaB degradation in vascular smooth muscle cells (VSMCs). UBA1 inhibition also leads to the accumulation of short-lived proteins such as p53, p21 and c-jun, which may account for the UBA1 inhibition-induced cell cycle delay. Thus, VSMCs proliferation is blocked. UBA1 inhibition effectively suppresses neointimal thickening through its anti-proliferative and anti-inflammatory effects |
744190 |
| 6.2.1.45 | malfunction |
mammary epithelial MCF-10A cells expressing shRNA against UBA6 fail in establishing cell cycle arrest in response to detachment from extracellular matrix, confluency with fully engaged cell-cell contact or growth factor deprivation. Moreover, UBA6-deficient MCF-10A cells undergo spontaneous epithelial-mesenchymal transition (EMT) under growth factor deprivation and exhibit accelerated kinetics of TGF-beta-induced EMT. UBA6 knockdown perturbs acinar morphogenesis and leads to formation of gigantic cell aggregates in mammary epithelial 3-D culture. UBA6 depletion suppresses contact innhibition of the cell cycle. UBA6 downregulation promotes cancer progression such as EMT and invasion in a population of human breast cancers |
745952 |
| 6.2.1.45 | malfunction |
the LMO2 protein interacts with the E1 ubiquitin-activating enzyme UBA6 at the C-terminal ubiquitin fold domain (UFD), which mediates the recognition and recruitment of the E2-conjugating enzyme USE1. Functionally, the LMO2-UBA6 interaction disturbes the interaction between UBA6 and USE1 and leads to the decline of the overall cellular FAT10ylation level as well as the FAT10ylation and degradation of a known FAT10 substrate p62 |
744237 |
