2.3.2.8: arginyltransferase
This is an abbreviated version!
For detailed information about arginyltransferase, go to the full flat file.
Word Map on EC 2.3.2.8
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2.3.2.8
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arginylation
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2.5.1.18
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rx:glutathione
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rx
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n-degrons
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polyubiquitylates
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medicine
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agriculture
- 2.3.2.8
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arginylation
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2.5.1.18
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rx:glutathione
- rx
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n-degrons
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polyubiquitylates
- medicine
- agriculture
Reaction
Synonyms
Arg-transferase, Arg-tRNA transferase, Arg-tRNA-protein transferase, Arg-tRNA-proteintransferase, arginyl transferase, arginyl tRNA transferase, arginyl-transfer ribonucleate-protein aminoacyltransferase, arginyl-transfer ribonucleate-protein transferase, arginyl-transferase, arginyl-tRNA protein transferase, arginyl-tRNA--protein transferase, arginyl-tRNA--protein transferase 1, arginyl-tRNA-protein transferase, arginyl-tRNA-protein transferase 1, arginyl-tRNA:protein arginyltransferase, arginyltransferase, arginyltransferase 1, ATE, Ate1, ATE1-1, ATE1-2, Ate1-3, Ate1-4, ATE1-encoded R-transferase, DdAte1, L-arginyltransferase, R-transferase
ECTree
2.3.2.8 arginyltransferaseAdvanced search results
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results (Engineering
Engineering on EC 2.3.2.8 - arginyltransferase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
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
Y416A
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no effect on Asp-containing substrate, but affects Glu-containing substrate
additional information
additional information
generation of RAP2.12 stabilization in ate1 ate2 double-null mutant plant lines
additional information
knockout of the gene encoding Ate1 and analysis of ate1- null cell phenotype, overview. Actin cytoskeleton dynamics by live-cell microscopy indicated significant changes in comparison to wild-type cells. In two-dimensional chemotaxis assays toward folate or cAMP, the motility of ate1-null cells is increased, while in three-dimensional chemoxadtaxis involving more confined conditions, the motility of ate1-null cells is significantly rexadduced. Actin isolated from ate1-null cells reveals different isoelectric properties and lower polymerization capacity in comparison to actin from wild-type
additional information
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knockout of the gene encoding Ate1 and analysis of ate1- null cell phenotype, overview. Actin cytoskeleton dynamics by live-cell microscopy indicated significant changes in comparison to wild-type cells. In two-dimensional chemotaxis assays toward folate or cAMP, the motility of ate1-null cells is increased, while in three-dimensional chemoxadtaxis involving more confined conditions, the motility of ate1-null cells is significantly rexadduced. Actin isolated from ate1-null cells reveals different isoelectric properties and lower polymerization capacity in comparison to actin from wild-type
additional information
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knockout of the gene encoding Ate1 and analysis of ate1- null cell phenotype, overview. Actin cytoskeleton dynamics by live-cell microscopy indicated significant changes in comparison to wild-type cells. In two-dimensional chemotaxis assays toward folate or cAMP, the motility of ate1-null cells is increased, while in three-dimensional chemoxadtaxis involving more confined conditions, the motility of ate1-null cells is significantly rexadduced. Actin isolated from ate1-null cells reveals different isoelectric properties and lower polymerization capacity in comparison to actin from wild-type
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additional information
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
additional information
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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
additional information
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
additional information
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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
additional information
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
additional information
Mus musculus 129SvEv/C57BL/6
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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
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additional information
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
additional information
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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
additional information
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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
additional information
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knockout or knockdown of ATE1 decreasing cellular sensitivity towards stressing conditions, e.g. heat, high NaCl, or H2O2
additional information
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knockout or knockdown of ATE1 decreasing cellular sensitivity towards stressing conditions, e.g. heat, high NaCl, or H2O2
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