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Aminoacyl-tRNA synthetases are a class of enzymes that charge tRNAs with their cognate amino acids. Additionally we are shipping Histidyl TRNA Synthetase Antibodies (74) and Histidyl TRNA Synthetase Proteins (21) and many more products for this protein.
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This study suggests that the human HisRS genes, while descending from a common ancestor with dual function for both types of tRNA(His), have acquired highly specialized tRNA recognition properties through evolution.
Despite the similar kinetics, differential scanning fluorimetry revealed that Y454S is less thermally stable than Wild Type HARS, and cells from Y454S patients grown at elevated temperatures demonstrate diminished levels of protein synthesis compared to those of Wild Type cells. The thermal sensitivity associated with the Y454S mutation represents a biochemical basis for understanding Usher Syndrome Type IIIB.
Loss of function mutations in histidyl-tRNA synthetase cause a spectrum of inherited peripheral neuropathies
Data suggest that by comparing human and trypanosomatid histidyl-tRNA synthetases (HisRS) may provide opportunities for developing specific inhibitors of Trypanosoma brucei HisRS.
Secreted histidyl-tRNA synthetase splice variants elaborate major epitopes for autoantibodies in inflammatory myositis.
Data indicate that higher anti-Jo1 levels were associated with disease severity in antisynthetase syndrome (ASS (show ASS1 ELISA Kits)) patients.
Findings suggest that histidyl-tRNA synthetase (HARS) is associated with axonal peripheral neuropathy.
Study identified sequence variants in the known disease-causing genes SLC6A3 (show SLC6A3 ELISA Kits) and FLVCR1 (show FLVCR1 ELISA Kits), and present evidence to strongly support the pathogenicity of variants identified in TUBGCP6 (show TUBGCP6 ELISA Kits), BRAT1 (show C7orf27 ELISA Kits), SNIP1 (show SNIP1 ELISA Kits), CRADD (show CRADD ELISA Kits), and HARS.
genomic organization of the HARS locus and mapping of transcripts originating from a bi-directional promoter controlling the differential expression of these gene
Demonstrating histidyl-tRNA synthetase (Jo-1)-specific T cell responses represents a key step in establishing the hypothesis that Jo-1 drives T cell-mediated autoimmunity in Jo-1+ polymyositis.
AA 60-90 of HRS were absolutely required for in vitro as well as in vivo signaling via MyD88 (show MYD88 ELISA Kits)-dependent TLR pathways to case myositis.
Aminoacyl-tRNA synthetases are a class of enzymes that charge tRNAs with their cognate amino acids. The protein encoded by this gene is a cytoplasmic enzyme which belongs to the class II family of aminoacyl-tRNA synthetases. The enzyme is responsible for the synthesis of histidyl-transfer RNA, which is essential for the incorporation of histidine into proteins. The gene is located in a head-to-head orientation with HARSL on chromosome five, where the homologous genes share a bidirectional promoter. The gene product is a frequent target of autoantibodies in the human autoimmune disease polymyositis/dermatomyositis. Several transcript variants encoding different isoforms have been found for this gene.
, histidine translase
, histidine--tRNA ligase, cytoplasmic
, histidine tRNA ligase
, histidyl-tRNA synthetase, cytoplasmic
, dead end homolog 1
, Histidyl-tRNA synthetase, cytoplasmic