Lane 1: Hela
Lane 2: A431
Lane 3: MCF-7
Lane 4: 293
Lane 5: Rat kidney
Lane 6: Rat brain
Lane 7: Mouse testis
Lane 8: Mouse colon
Recombinant Rabbit monoclonal primary
Recombinant HPRT Monoclonal Antibody (ET1706-08)
MCF-7 cell lysate, 293 cell lysate, Hela cell lysate, A431 cell lysate, rat kidney tissue lysate, rat tonsil brain lysate, mouse testis tissue lysate, mouse colon tissue lysate, zebrafish tissue lysates, rat brain tissue, human tonsil tissue, human colon carcinoma tissue, human kidney tissue.
Store at +4C after thawing. Aliquot store at -20C or -80C. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein A affinity purified.
HGPRT antibody; HGPRTase antibody; HPRT 1 antibody; HPRT_HUMAN antibody; HPRT1 antibody; Hypoxanthine guanine phosphoribosyltransferase antibody; Hypoxanthine phosphoribosyltransferase 1 (Lesch Nyhan syndrome) antibody; Hypoxanthine phosphoribosyltransferase 1 antibody; Hypoxanthine-guanine phosphoribosyltransferase antibody
Belongs to the purine/pyrimidine phosphoribosyltransferase family.
HPRT (hypoxanthine phosphoribosyltransferase 1), also known as HGPRT or HPRT1, is a 218 amino acid cytoplasmic protein that belongs to the purine/pyrimidine phosphoribosyltransferase family. Involved in purine metabolism, HPRT functions as a purine salvage enzyme that catalyzes the conversion of hypoxathine and guanine to their respective mononucleotides (inosine monophosphate and guanosine monophosphate, respectively). HPRT exists as a homotetramer that can bind two magnesium ions as cofactors. Defects in the gene encoding HPRT are the cause of gout and Lesch-Nyhan syndrome (LNS), both of which are characterized by a partial or complete lack of NPRT enzymatic activity. While a partial loss of HPRT enzymatic activity results in a buildup of uric acid (gout), a total loss of enzymatic activity results in hyperuricaemia, mental retardation, choreoathetosis and compulsive self-mutilation, all of which are symptoms associated with LNS. The severity of these diseases suggests an essential role for HPRT in purine metabolism.