PARK7
PARK7 (parkinsonism associated deglycase, also known as DJ-1, DJ1 and GATD2) is a multifunctional protein that protects cells against oxidative stress and cell death. It acts as an oxidative stress sensor and redox-sensitive chaperone, and has been described as a deglycase. Browse Assay Genie's current range of PARK7 research reagents below, or read on for the biology behind the target.
PARK7 is a multifunctional protein whose precise molecular function is described as controversial. It plays an important role in protecting cells from oxidative stress and cell death, acting as an oxidative stress sensor and as a redox-sensitive chaperone and protease. It eliminates hydrogen peroxide and protects cells against hydrogen peroxide-induced cell death, and it is required for correct mitochondrial morphology and function and for autophagy of dysfunctional mitochondria. It also binds copper and toxic mercury ions, which enhances cell protection against metal toxicity.
PARK7 has been described as a protein and nucleotide deglycase. In this role it repairs methylglyoxal- and glyoxal-glycated proteins by acting on early glycation intermediates, which prevents the formation of irreversible advanced glycation endproducts. It is also reported to repair glycated guanine in the free nucleotide pool, DNA and RNA, as part of a guanine glycation repair system, and to protect histones from methylglyoxal adduction. Other work disputes this deglycase function. PARK7 also stabilises NFE2L2 and PINK1 in neuroprotective mechanisms, modulates NF-kappa-B signalling, and positively regulates androgen signalling. In macrophages it interacts with the NADPH oxidase subunit NCF1 to direct reactive oxygen species production.
The PARK7 gene product belongs to the peptidase C56 family and to the HGNC group of glutamine amidotransferase class 1 domain containing proteins. UniProt records it in the cell membrane, cytoplasm, nucleus, membrane rafts, mitochondrion and endoplasmic reticulum. Earlier names were Parkinson disease (autosomal recessive, early onset) 7 and parkinson protein 7, reflecting that defects in the gene cause autosomal recessive early-onset Parkinson disease 7. Two transcript variants encode the same protein.
Defects in the PARK7 gene cause autosomal recessive early-onset Parkinson disease 7, and the protein supports neuroprotective mechanisms including stabilisation of PINK1.
PARK7 senses oxidative stress, eliminates hydrogen peroxide and protects cells against hydrogen peroxide-induced death.
Reported deglycase activity on proteins, nucleotides, nucleic acids and histones makes PARK7 a focus for studies of methylglyoxal and glyoxal damage.
PARK7 supports mitochondrial morphology, mitophagy and reactive oxygen species control, including in pancreatic islets where it helps maintain glucose homeostasis.
PARK7 protects cells against oxidative stress and cell death, acting as an oxidative stress sensor and redox-sensitive chaperone. It has also been described as a protein and nucleotide deglycase, though that activity is disputed. It supports mitochondrial function and regulates androgen and NF-kappa-B signalling.
Yes. DJ-1, DJ1 and GATD2 are aliases of PARK7, and UniProt lists the protein as Parkinson disease protein 7. Earlier HGNC names were Parkinson disease (autosomal recessive, early onset) 7 and parkinson protein 7. Two transcript variants encode the same protein.
Defects in the PARK7 gene cause autosomal recessive early-onset Parkinson disease 7. Orthologues exist in mouse and rat, both named Park7, so the protein can be studied in rodent models; check the datasheet of any product for its validated reactivity.
Partners of PARK7 in mitochondrial quality control, oxidative stress signalling and neuroprotection.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q99497; product specifications from Assay Genie datasheets.