HARS Antibody

Code CSB-PA546948
Size US$297
Order now
Image
  • Western blot analysis of extracts from HeLa cells, using HARS antibody.
  • Immunofluorescence analysis of HepG2 ells, using HARS antibody.
Have Questions? Leave a Message or Start an on-line Chat

Product Details

Full Product Name
Rabbit anti-Homo sapiens (Human) HARS Polyclonal antibody
Uniprot No.
Target Names
HARS
Alternative Names
cytoplasmic antibody; EC 6.1.1.21 antibody; FLJ20491 antibody; HARS antibody; HisRS antibody; Histidine tRNA ligase, cytoplasmic antibody; histidine translase antibody; Histidine tRNA ligase antibody; Histidine--tRNA ligase antibody; Histidyl tRNA synthetase antibody; Histidyl-tRNA synthetase antibody; HRS antibody; Human histidyl tRNA synthetase homolog (HO3) mRNA complete cds antibody; SYHC_HUMAN antibody; USH3B antibody
Raised in
Rabbit
Species Reactivity
Human,Mouse
Immunogen
Synthesized peptide derived from C-terminal of Human HARS.
Immunogen Species
Homo sapiens (Human)
Clonality
Polyclonal
Purification Method
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration
It differs from different batches. Please contact us to confirm it.
Form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Tested Applications
ELISA,WB,IF
Recommended Dilution
Application Recommended Dilution
WB 1:500-1:3000
IF 1:100-1:500
Troubleshooting and FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time
Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

Customer Reviews and Q&A

 Customer Reviews

There are currently no reviews for this product.

Submit a Review here

Target Background

Function
Catalyzes the ATP-dependent ligation of histidine to the 3'-end of its cognate tRNA, via the formation of an aminoacyl-adenylate intermediate (His-AMP). Plays a role in axon guidance.
Gene References into Functions
  1. 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. PMID: 28321488
  2. 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. PMID: 28632987
  3. Loss of function mutations in histidyl-tRNA synthetase cause a spectrum of inherited peripheral neuropathies PMID: 26072516
  4. Data suggest that by comparing human and trypanosomatid histidyl-tRNA synthetases (HisRS) may provide opportunities for developing specific inhibitors of Trypanosoma brucei HisRS. PMID: 25151410
  5. Secreted histidyl-tRNA synthetase splice variants elaborate major epitopes for autoantibodies in inflammatory myositis. PMID: 24898250
  6. Data indicate that higher anti-Jo1 levels were associated with disease severity in antisynthetase syndrome (ASS) patients. PMID: 24286268
  7. Non-Jo-1 anti-synAb positive patients have decreased survival compared with Jo-1 patients. PMID: 23422076
  8. Findings suggest that histidyl-tRNA synthetase (HARS) is associated with axonal peripheral neuropathy. PMID: 22930593
  9. The crystal structure of a novel splice variant of a tRNA synthetase lacking the entire catalytic domain. PMID: 22958643
  10. Although anti-Jo1 positive patients with antisynthetase syndrome share features of patients with anti-PL7/PL12 antibody, they exhibit many differences regarding clinical phenotype and long-term outcome. PMID: 22326685
  11. Study identified sequence variants in the known disease-causing genes SLC6A3 and FLVCR1, and present evidence to strongly support the pathogenicity of variants identified in TUBGCP6, BRAT1, SNIP1, CRADD, and HARS. PMID: 22279524
  12. genomic organization of the HARS locus and mapping of transcripts originating from a bi-directional promoter controlling the differential expression of these gene PMID: 12056811
  13. 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. PMID: 12471150
  14. the TSG101 interaction with HRS is a crucial step in endocytic down-regulation of mitogenic signaling and this interaction may have a role in linking the functions of early and late endosomes PMID: 12802020
  15. A proteolytically sensitive conformation of HisRS exists in the lung, the target tissue associated with this autoantibody response. PMID: 17665459
  16. clinical and prognostic profiles of 45 patients displaying anti-histidyl-tRNA synthetase autoantibodies were determined PMID: 17785330

Show More

Hide All

Involvement in disease
Usher syndrome 3B (USH3B); Charcot-Marie-Tooth disease 2W (CMT2W)
Subcellular Location
Cytoplasm.
Protein Families
Class-II aminoacyl-tRNA synthetase family
Tissue Specificity
Brain, heart, liver and kidney.
Database Links

HGNC: 4816

OMIM: 142810

KEGG: hsa:3035

STRING: 9606.ENSP00000425634

UniGene: Hs.528050

icon of phone
Call us
301-363-4651 (Available 9 a.m. to 5 p.m. CST from Monday to Friday)
icon of address
Address
7505 Fannin St., Ste 610, Room 7 (CUBIO Innovation Center), Houston, TX 77054, USA
icon of social media
Join us with

Subscribe newsletter

Leave a message

* To protect against spam, please pass the CAPTCHA test below.
CAPTCHA verification
© 2007-2024 CUSABIO TECHNOLOGY LLC All rights reserved. 鄂ICP备15011166号-1
webinars: DT3C facilitates antibody internalization X
Place an order now

I. Product details

*
*
*
*

II. Contact details

*
*

III. Ship To

*
*
*
*
*
*
*

IV. Bill To

*
*
*
*
*
*
*
*