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Results 1 - 10 of 51 > >>
EC Number General Information Commentary Reference
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8evolution arginyltransferase (ATE1) is an evolutionary conserved enzyme 760135
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8evolution ATE1 Arg-transferase is an evolutionarily conserved protein present in all eukaryotes from fungi to animals -, 758964
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8evolution eukaryotic systems including Saccharomyces cerevisiae (budding yeast), mouse cells, and human cells, all contain the evolutionarily conserved ATE1 gene -, 759021
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8evolution plant ATEs and their evolutionary relationship with other ATEs, overview. Identification of two Arabidopsis thaliana Nt-amidases mediating recognition of tertiary destabilizing Nt-amino acids Asn and Gln have shown that the N-end rule pathway in plants is very similar to that in animals, highlighting a possible evolutionary common origin. But the steps related to protein degradation likely evolved after plant and animal divergence, as suggested by the differences in PRTs and UBR N-recognins. Plant evolutionary analysis has identified ATE orthologous genes from the green alga Chlamydomonas reinhardtii to angiosperms. In general, only one ATE gene is detected in a given plant species, with the two conserved ATE domains located at the N- and C-termini. Some species, such as Arabidopsis, Populus, and Sorghum, have experienced gene duplication 759302
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8evolution the Dictyostelium discoideum genome encodes only one Ate1 family member, Ate1 (DdAte1) -, 759753
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8malfunction Ate1- null cells are almost completely lacking focal actin adhesion sites at the substrate-attached surface and are only weakly adhesive. In vitro polymerization assays with actin purified from ate1-null cells reveal a diminished polymerization capacity in comparixadson to wild-type actin. Chemotaxis of aggregation-competent ate1-/- null cells is impaired in three-dimensional compared with two-dimensional environments -, 759753
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8malfunction ATE1-null mice show severe intracerebral hemorrhages and cystic space near the neural tubes. The ATE1-/- brain shows defective G-protein signaling. Reduced mitosis in ATE1-/- neuroepithelium and a significantly higher nitric oxide concentration in ATE1-/- brain are observed. In ATE1-null murine embryos, neural-tube genesis is severely defective, and this problem may be the primary cause of embryonic mortality of the mutant mice. ATE1 expression is more prominent in the embryonic brain and spinal cord than in the heart. ATE1-null embryonic brain shows stabilized regulators of G protein signaling (RGS) proteins, defective G protein signaling, and a higher concentration of NO. Proliferation of ATE1-/- neuroepithelial cells in the developing primary neural tube is significantly impaired. Stabilized RGS proteins in ATE1-null mice and reduced activities of downstream effectors, overview -, 758964
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8malfunction blocking the Arg/N-end rule pathway significantly impaired the fusion of autophagosomes with lysosomes. The inhibition of the Arg/N-end rule pathway with para-chloroamphetamine (PCA) significantly elevates levels of MAPT and huntingtin aggregates, accompanied by increased numbers of LC3 and SQSTM1 puncta. Cells treated with the Arg/N-end rule inhibitor become more sensitized to proteotoxic stress-induced cytotoxicity. Treatment with PCA delays the fusion of autophagosomes with lysosomes and leads to the accumulation of autophagic markers 758714
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8malfunction blocking the Arg/N-end rule pathway significantly impaired the fusion of autophagosomes with lysosomes. The inhibition of the Arg/N-end rule pathway with para-chloroamphetamine (PCA) significantly elevates levels of MAPT and huntingtin aggregates, accompanied by increased numbers of LC3 and SQSTM1 puncta. Cells treated with the Arg/N-end rule inhibitor become more sensitized to proteotoxic stress-induced cytotoxicity. Treatment with PCA delays the fusion of autophagosomes with lysosomes and leads to the accumulation of autophagic markers. The direct targets of PCA are UBR1 and UBR2 proteins, not ATE1, an upstream component of the Arg/N-end rule pathway 758714
Display the word mapDisplay the reaction diagram Show all sequences 2.3.2.8malfunction conditional knockout mice with Ate1 deletion in the nervous system driven by Nestin promoter (Nes-Ate1 mice) are weaker than wild-type mice, resulting in low postnatal survival rates, and have abnormalities in the brain that suggest defects in neuronal migration. Cultured Ate1 knockout neurons show a reduction in the neurite outgrowth and the levels of doublecortin and F-actin in the growth cones. A lack of beta-actin arginylation leads to a marked reduction in growth cone spreading, accompanied by the corresponding decrease in the actin polymer. 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. Complete Ate1 knockout mice die at E12.5-E14.5 during development 759108
Results 1 - 10 of 51 > >>