Human GRS ELISA Kit

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  • Catalog
    E017238
  • species
    Human
  • GeneGRS
  • Standard CurveHuman GRS ELISA Kit
  • SpecificityThis kit exhibits no detectable cross-reactivity with HRS, KRS, NRS, SRS, WRS, YRS and AIMP1
  • SamplesSerum, Plasma , tissue homogenates,Cell culture supernates,Other biological fluids.
  • SensitivityThe minimum detectable dose of GRS was determined by two standard deviations to the mean value of 20 blank samples. The minimum detectable dose of human GRS using a standard curve generated is 6 ng/ml.
  • Intended UseHuman GRS ELISA Kit allows for the in vitro quantitative determination of GRS , concentrations in serum, Plasma , tissue homogenates and Cell culture supernates and Other biological fluids.
  • StorageFor 5-7days:Store the whole kit at 4℃
    For a Long time :Store the Substrate at 4℃, other reagent should store at -20℃.
  • Product Categories/FamilyCytokines & Cell Signalling; Oncology; Research Assays; Assay Categories
  • Product Description
    specifical
    Background: GRS ELISA kit applies a technique called sandwich immunoassay. The microtiter plate provided in this kit has been pre-coated with a monoclonal antibody fragments specific for GRS. This GRS ELISA kit is to be used for the determination of GRS in human serum and cell lysate. As ancient proteins that arose as part of the development of the genetic code, aminoacyl-tRNA synthetases (ARSs) are essential components of the translation apparatus. The 20 enzymes, 1 for each amino acid, catalyze the attachment of each amino acid to its cognate tRNA in the cytoplasm, where the charged tRNAs are then used for ribosomal protein synthesis(1). Glycyl-tRNA synthetase (GRS) autoantibodies were detected in serum of subjects with cancer(2). In part because of our ongoing investigations of its novel functions, we focused on GRS. GRS can be secreted from macrophages in response to Fas ligand that is released from tumor cells. Through cadherin (CDH)6 (K-cadherin), GRS bound to different ERK-activated tumor cells, and released phosphatase 2A (PP2A) from CDH6. The activated PP2A then suppressed ERK signaling through dephosphorylation of ERK and induced apoptosis.With in vivo administration of GRS, growth of tumors with a high level of CDH6 and ERK activation were strongly suppressed. These observations led us to attempt to understand a potential role for GRS as a secreted protein in a cancer microenvironment (3).



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