DJ-1/PARK7 (human, recombinant)

DJ-1/PARK7 (human, recombinant)

CAT N°: 23589
Price:

€550.00 €467.50

DJ-1/Parkinson disease protein 7 (PARK7) is a dimeric protein deglycase that repairs methylglyoxal- and glyoxal-glycated cysteine, arginine, and lysine residues in oxidatively damaged proteins.{37402} It acts on early glycation intermediates (hemithioacetals and aminocarbinols) to prevent the formation of irreversibly damaged advanced glycation end products (AGEs). PARK7 also repairs methylglyoxal- and glyoxal-glycated dGTP, GTP, GDP, GMP, RNA, and DNA.{35071} Knockdown of PARK7 in vitro increases glycated DNA, DNA strand breaks, and phosphorylated p53 levels but decreases mRNA expression of the antioxidant-related enzyme NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1) and destabilizes the nuclear factor erythroid 2-related factor (Nrf2), a master regulator of antioxidant transcriptional responses.{37406} . PARK7 is also a glyoxalase that converts glyoxal and methylglyoxal to glycolic and lactic acid, respectively, in the absence of glutathione.{37403} It acts as a redox-sensitive molecular chaperone and inhibits aggregation of ?-synuclein in cell-free assays and in murine neuroblastoma cells.{37404} PARK7 forms a complex with the E3 ubiquitin ligase Parkin and PTEN-induced putative kinase 1 (PINK1) that promotes ubiquitination and degradation of Parkin substrates, including Parkin itself and Synphilin-1 in neuroblastoma SH-SY5Y cells and human brain lysates.{37405} Mutations to PARK7 have been linked to autosomal recessive, early-onset Parkinson’s disease.{37407}

Territorial Availability: Available through Bertin Technologies only in France

  • Correlated keywords
    • HELS67p GATD-2 Nrf-2 p-53 d-GTP PARK-7 SHSY5Y Oncogene DJ1 Epididymis Secretory Sperm Binding Protein Li 67p Parkinsonism-Associated EC 3.5.1.124 3.1.2- EC3.1.2- EC3.5.1.124 HEL-S-67p GATD2 anti-oxidant NQO-1 PINK-1
  • Product Overview:
    DJ-1/Parkinson disease protein 7 (PARK7) is a dimeric protein deglycase that repairs methylglyoxal- and glyoxal-glycated cysteine, arginine, and lysine residues in oxidatively damaged proteins.{37402} It acts on early glycation intermediates (hemithioacetals and aminocarbinols) to prevent the formation of irreversibly damaged advanced glycation end products (AGEs). PARK7 also repairs methylglyoxal- and glyoxal-glycated dGTP, GTP, GDP, GMP, RNA, and DNA.{35071} Knockdown of PARK7 in vitro increases glycated DNA, DNA strand breaks, and phosphorylated p53 levels but decreases mRNA expression of the antioxidant-related enzyme NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1) and destabilizes the nuclear factor erythroid 2-related factor (Nrf2), a master regulator of antioxidant transcriptional responses.{37406} . PARK7 is also a glyoxalase that converts glyoxal and methylglyoxal to glycolic and lactic acid, respectively, in the absence of glutathione.{37403} It acts as a redox-sensitive molecular chaperone and inhibits aggregation of ?-synuclein in cell-free assays and in murine neuroblastoma cells.{37404} PARK7 forms a complex with the E3 ubiquitin ligase Parkin and PTEN-induced putative kinase 1 (PINK1) that promotes ubiquitination and degradation of Parkin substrates, including Parkin itself and Synphilin-1 in neuroblastoma SH-SY5Y cells and human brain lysates.{37405} Mutations to PARK7 have been linked to autosomal recessive, early-onset Parkinson’s disease.{37407}

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