Glutathione Synthetase Recombinant Rabbit monoclonal Antibody IgG

SKU: BA112534-100µl

Fig1: Western blot analysis of Glutathione Synthetase on different lysates using anti-Glutathione Synthetase antibody at 1/500 dilution.

  Positive control:

  Lane 1: SiHa

  Lane 2: Mouse colon

  Lane 3: Rat liver


Fig2: ICC staining Glutathione Synthetase in LOVO cells (green). The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.

Fig3: Immunohistochemical analysis of paraffin-embedded human tonsil tissue using anti-Glutathione Synthetase antibody. Counter stained with hematoxylin.

Bon Opus Cat. #BA112534
  • Host Species; Species Reactivity

    Rabbit; Human, Mouse, Rat
  • Immunogen

    Recombinant protein
  • Application Summary

  • Purification; Formulation

    ProA affinity purified; 1*TBS (pH7.4), 1%BSA, 40%Glycerol. Preservative: 0.05% Sodium Azide.; Liquid form.
  • ALTnames

    Glutathione synthetase, Glutathione synthase
  • Background

    GSS (Glutathione synthetase) is a 474 amino acid protein encoded by the gene located at human chromosome 20q11.2. GSS consists of three loops projecting from an antiparallel β-sheet, a parallel β-sheet and a lid of anti-parallel sheets, which provide access to the ATP-binding site. Although Southern blot and gene analysis suggest that GSS may be the only member of a unique family, the crystal structure indicates that GSS belongs to the ATP-GRASP superfamily. GSS is expressed in hemocytes and nucleated cells, including the brain. GSS occurs as a homodimer. There are two steps in the production of Glutathione, begining with γ-GCS and ending with GSS. In an ATP-dependent reaction, GSS produces Glutathione from γ-glutamylcysteine and glycine precursors. Partial hepatectomy, diethyl maleate, buthionine sulfoximine, tert-butylhaydroquinone and thioacetamide increase the ex-pression of GSS, which causes an increase in Glutathione levels. An inherited autosomal recessive disorder, 5-oxoprolinuria (pyroglutamic aciduria), is caused by GSS deficiencies, which leads to central nervous system damage, hemolytic anemia, metabolic acidosis and urinary excretion of 5-oxoproline.(ET7107-62)

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