EC Number   |
General Information |
Reference |
|---|
    6.1.1.21 | evolution |
a conserved tRNA recognition pattern change during evolution leading to a divergent orthogonal HisRS/tRNAHis pair |
716383 |
| 6.1.1.21 | evolution |
phylogenetic analysis reveals that tRNAThr1 originated from tRNAHis |
716387 |
| 6.1.1.21 | evolution |
significantly different rate enhancements by four HisRS urzymes demonstrate that amino acid activation provides an experimental metric for recapitulating very early evolutionary events. Catalytic activities of HisRS-1 and HisRS-2 provide complementary support for Rodin-Ohno hypothesis that ancestral class I and II aaRS were encoded on opposite strands of same gene |
715579 |
| 6.1.1.21 | evolution |
the conserved active site residues near the reaction center, Thr60, Val62, Pro82, Glu83, Gly84, Arg113, Gln127, Arg259, Gly260, Leu261, Ala284 and Ala306, which have a major role in the reaction mechanism and catalysis, retain their specific position and orientation relative to the substrate in the three species, Escherichia coli, Thermus thermophilus, and Staphylococcus aureus, modelling, reaction emchanism, detailed overview |
714477 |
| 6.1.1.21 | evolution |
the conserved active site residues near the reaction center, Thr60, Val62, Pro82, Glu83, Gly84, Arg113, Gln127, Arg259, Gly260, Leu261, Ala284 and Ala306, which have a major role in the reaction mechanism and catalysis, retain their specific position and orientation relative to the substrate in the three species, Escherichia coli, Thermus thermophilus, and Staphylococcus aureus, modelling, reaction mechanism, detailed overview |
714477 |
| 6.1.1.21 | malfunction |
mutations in histidyl-tRNA synthetase cause the dominant axonal peripheral neuropathy Charcot-Marie-Tooth disease type 2W |
745058 |
| 6.1.1.21 | malfunction |
mutations in the tRNAHis anticodon cause a drastic loss of in vitro histidylation, and mutations of bases A73 and U72 also reduce charging |
716383 |
| 6.1.1.21 | malfunction |
the loss of fertility caused by hars-1 RNAi is partially mediated by apoptosis. Complete loss of hars-1 using the hars-1(tm4074) null allele. Homozygous hars-1 (tm4074) animals arrest development as L2 larvae, as determined by overall body size and by extent of gonad development, overview |
716785 |
| 6.1.1.21 | more |
in idiopathic inflammatory myopathy, the aminoacyl-transfer RNA synthetases are targets of the autoimmune response. Among these antigens, antibodies against histidyl-transfer RNA synthetase are by far the most prominent found in 15-20% of myositis patients, and more strikingly, are detected in about 70% of patients with myositis and interstitial lung disease. Strong association of HisRS with interstitial lung disease in humans |
713999 |
| 6.1.1.21 | more |
mouse HisRS without adjuvant, containing Toll-like receptor TLR-4, can induce sustained muscle inflammation and an adaptive immune response to HisRS. Mice lacking TLR-4 show that the ability of mouse HisRS to produce muscle inflammation does not require TLR-4 signaling, nor is it dependent on recognition of B cell and T cell receptors. When TLR-4-deficient animals are immunized with HisRS, they have a preserved inflammatory response in muscle but fail to generate a HisRS antibody response |
713999 |
