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Western blot of mouse adipose tissue showing specific immunolabeling of the ~25k DsbA-L protein using DsbA-L antibody (GTX82705).
Western blot of mouse adipose tissue showing specific immunolabeling of the ~25k DsbA-L protein using DsbA-L antibody (GTX82705).
Western blot of mouse adipose tissue showing specific immunolabeling of the ~25k DsbA-L protein using DsbA-L antibody (GTX82705).

Glutathione S-transferase kappa 1 antibody

GTX82705
GeneTex
ApplicationsImmunoFluorescence, Western Blot, ImmunoCytoChemistry, ImmunoHistoChemistry
Product group Antibodies
ReactivityHuman, Mouse
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Overview

  • Supplier
    GeneTex
  • Product Name
    Glutathione S-transferase kappa 1 antibody
  • Delivery Days Customer
    9
  • Application Supplier Note
    Optimal working dilutions should be determined experimentally by the end user.
  • Applications
    ImmunoFluorescence, Western Blot, ImmunoCytoChemistry, ImmunoHistoChemistry
  • Certification
    Research Use Only
  • Clonality
    Polyclonal
  • Conjugate
    Unconjugated
  • Host
    Rabbit
  • Isotype
    IgG
  • Scientific Description
    Disulfide-bond-A oxidoreductase-like protein (DsbA-L, previously named as GST Kappa) is an adiponectin-interacting protein. DsbA-L is highly expressed in adipose tissue, and its expression level is negatively correlated with obesity in mice and humans. DsbA-L expression in 3T3-L1 adipocytes is stimulated by the insulin sensitizer rosiglitazone and inhibited by the inflammatory cytokine TNFalpha. Polymorphism of DsbA-L gene has recently been implicated in insulin secretion and body fat distribution. Overexpression of DsbA-L promotes adiponectin multimerization while suppressing DsbA-L expression by RNAi markedly and selectively reduces adiponectin levels and secretion in 3T3-L1 adipocytes. Recent studies identify DsbA-L as a key regulator for adiponectin biosynthesis.
  • Reactivity
    Human, Mouse
  • Storage Instruction
    -20°C or -80°C,2°C to 8°C
  • UNSPSC
    12352203

References

  • Gao P, Yang M, Chen X, et al. DsbA-L deficiency exacerbates mitochondrial dysfunction of tubular cells in diabetic kidney disease. Clin Sci (Lond). 2020,134(7):677-694. doi: 10.1042/CS20200005
    Read this paper