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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 Proteins (21) and Histidyl TRNA Synthetase Kits (6) and many more products for this protein.
Showing 10 out of 73 products:
Human Polyclonal HARS Primary Antibody for IHC (p), WB - ABIN391819
Levine, Raben, Xie, Askin, Tuder, Mullins, Rosen, Casciola-Rosen: Novel conformation of histidyl-transfer RNA synthetase in the lung: the target tissue in Jo-1 autoantibody-associated myositis. in Arthritis and rheumatism 2007
Show all 2 references for 391819
Human Polyclonal HARS Primary Antibody for EIA, IHC (p) - ABIN359730
Lu, Hope, Brasch, Reinhard, Cohen: TSG101 interaction with HRS mediates endosomal trafficking and receptor down-regulation. in Proceedings of the National Academy of Sciences of the United States of America 2003
Show all 2 references for 359730
Human Polyclonal HARS Primary Antibody for ELISA, WB - ABIN561225
Chardonnet, Decottignies, Amar, Le Caer, Davis, Laroche, Le Maréchal: New mortalin and histidyl tRNA synthetase isoforms point out a pitfall in proteomic analysis of Egr1 genetically modified mice. in Proteomics 2007
Human Polyclonal HARS Primary Antibody for IF, ELISA - ABIN1533611
Tsui, Mok, de Souza, Martin, Tsui: Transcriptional analyses of the gene region that encodes human histidyl-tRNA synthetase: identification of a novel bidirectional regulatory element. in Gene 1993
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 Antibodies)) 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 Antibodies) and FLVCR1 (show FLVCR1 Antibodies), and present evidence to strongly support the pathogenicity of variants identified in TUBGCP6 (show TUBGCP6 Antibodies), BRAT1 (show C7orf27 Antibodies), SNIP1 (show SNIP1 Antibodies), CRADD (show CRADD Antibodies), 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 Antibodies)-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