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PARK7 blocking peptide

PARK7 Blocking Peptide (C-term)

Gene Names
PARK7; DJ1; DJ-1; HEL-S-67p
Synonyms
PARK7; PARK7 Blocking Peptide (C-term); Protein DJ-1; 34--; Oncogene DJ1; Parkinson disease protein 7; PARK7 blocking peptide
Ordering
Specificity
The synthetic peptide sequence is selected from aa 130-144 of HUMAN PARK7
Form/Format
Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.
Sequence Length
189
Cellular Location
Cell membrane; Lipid-anchor. Cytoplasm. Nucleus. Membrane raft. Mitochondrion. Note: Under normal conditions, located predominantly in the cytoplasm and, to a lesser extent, in the nucleus and mitochondrion. Translocates to the mitochondrion and subsequently to the nucleus in response to oxidative stress and exerts an increased cytoprotective effect against oxidative damage. Detected in tau inclusions in brains from neurodegenerative disease patients. Membrane raft localization in astrocytes and neuronal cells requires palmitoylation
Tissue Location
Highly expressed in pancreas, kidney, skeletal muscle, liver, testis and heart. Detected at slightly lower levels in placenta and brain. Detected in astrocytes, Sertoli cells, spermatogonia, spermatids and spermatozoa
Preparation and Storage
Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C.
Related Product Information for PARK7 blocking peptide
Protects cells against oxidative stress and cell death. Plays a role in regulating expression or stability of the mitochondrial uncoupling proteins SLC25A14 and SLC25A27 in dopaminergic neurons of the substantia nigra pars compacta and attenuates the oxidative stress induced by calcium entry into the neurons via L-type channels during pacemaking. Eliminates hydrogen peroxide and protects cells against hydrogen peroxide-induced cell death. Following removal of a C-terminal peptide, displays protease activity and enhanced cytoprotective action against oxidative stress-induced apoptosis. Stabilizes NFE2L2 by preventing its association with KEAP1 and its subsequent ubiquitination. Binds to OTUD7B and inhibits its deubiquitinating activity. Enhances RELA nuclear translocation. Binds to a number of mRNAs containing multiple copies of GG or CC motifs and partially inhibits their translation but dissociates following oxidative stress. Required for correct mitochondrial morphology and function and for autophagy of dysfunctional mitochondria. Regulates astrocyte inflammatory responses. Acts as a positive regulator of androgen receptor-dependent transcription. Prevents aggregation of SNCA. Plays a role in fertilization. Has no proteolytic activity. Has cell-growth promoting activity and transforming activity. May function as a redox-sensitive chaperone. May regulate lipid rafts-dependent endocytosis in astrocytes and neuronal cells.

NCBI and Uniprot Product Information

NCBI GI #
NCBI GeneID
UniProt Accession #
Molecular Weight
19,891 Da
NCBI Official Full Name
Protein deglycase DJ-1
NCBI Official Synonym Full Names
Parkinsonism associated deglycase
NCBI Official Symbol
PARK7
NCBI Official Synonym Symbols
DJ1; DJ-1; HEL-S-67p
NCBI Protein Information
protein deglycase DJ-1
UniProt Protein Name
Protein deglycase DJ-1
Protein Family
UniProt Gene Name
PARK7
UniProt Synonym Gene Names
DJ-1
UniProt Entry Name
PARK7_HUMAN

NCBI Description

The product of this gene belongs to the peptidase C56 family of proteins. It acts as a positive regulator of androgen receptor-dependent transcription. It may also function as a redox-sensitive chaperone, as a sensor for oxidative stress, and it apparently protects neurons against oxidative stress and cell death. Defects in this gene are the cause of autosomal recessive early-onset Parkinson disease 7. Two transcript variants encoding the same protein have been identified for this gene. [provided by RefSeq, Jul 2008]

Uniprot Description

DJ-1: associated with autosomal recessive early onset parkinsonism. Involved in the oxidative stress response. Three cysteines in DJ-1 may be oxidized to cysteine sulphonic acid in the cellular response to H2O2. Loss of DJ-1 function may lead to neurodegeneration.

Protein type: Tumor suppressor; Nuclear receptor co-regulator; Transcription regulation; EC 3.4.-.-

Chromosomal Location of Human Ortholog: 1p36.23

Cellular Component: axon; chromatin; cytoplasm; cytosol; mitochondrial respiratory chain complex I; mitochondrion; nucleus; PML body

Molecular Function: androgen receptor binding; copper ion binding; cytokine binding; double-stranded DNA binding; enzyme binding; glyoxalase III activity; identical protein binding; kinase binding; mercury ion binding; mRNA binding; oxidoreductase activity, acting on peroxide as acceptor; peptidase activity; protein binding; protein homodimerization activity; receptor binding; single-stranded DNA binding; superoxide dismutase copper chaperone activity; transcription coactivator activity; transcription factor binding

Biological Process: activation of protein kinase B; detoxification of copper ion; detoxification of mercury ion; glycolate biosynthetic process; hydrogen peroxide metabolic process; methylglyoxal catabolic process to D-lactate; mitochondrion organization and biogenesis; negative regulation of apoptosis; negative regulation of neuron apoptosis; negative regulation of proteasomal ubiquitin-dependent protein catabolic process; negative regulation of protein amino acid phosphorylation; negative regulation of protein binding; negative regulation of protein export from nucleus; negative regulation of protein kinase activity; negative regulation of protein sumoylation; negative regulation of protein ubiquitination; negative regulation of ubiquitin-protein ligase activity; positive regulation of interleukin-8 production; positive regulation of peptidyl-serine phosphorylation; positive regulation of protein kinase B signaling cascade; positive regulation of transcription factor activity; positive regulation of transcription from RNA polymerase II promoter; protein deglycosylation; protein stabilization; Ras protein signal transduction; regulation of inflammatory response; regulation of mitochondrial membrane potential; regulation of neuron apoptosis; regulation of TRAIL receptor biosynthetic process

Disease: Parkinson Disease 7, Autosomal Recessive Early-onset

Research Articles on PARK7

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Product Notes

The PARK7 park7 (Catalog #AAA9229295) is a Blocking Peptide and is intended for research purposes only. The product is available for immediate purchase. It is sometimes possible for the material contained within the vial of "PARK7, Blocking Peptide" to become dispersed throughout the inside of the vial, particularly around the seal of said vial, during shipment and storage. We always suggest centrifuging these vials to consolidate all of the liquid away from the lid and to the bottom of the vial prior to opening. Please be advised that certain products may require dry ice for shipping and that, if this is the case, an additional dry ice fee may also be required.

Precautions

All products in the AAA Biotech catalog are strictly for research-use only, and are absolutely not suitable for use in any sort of medical, therapeutic, prophylactic, in-vivo, or diagnostic capacity. By purchasing a product from AAA Biotech, you are explicitly certifying that said products will be properly tested and used in line with industry standard. AAA Biotech and its authorized distribution partners reserve the right to refuse to fulfill any order if we have any indication that a purchaser may be intending to use a product outside of our accepted criteria.

Disclaimer

Though we do strive to guarantee the information represented in this datasheet, AAA Biotech cannot be held responsible for any oversights or imprecisions. AAA Biotech reserves the right to adjust any aspect of this datasheet at any time and without notice. It is the responsibility of the customer to inform AAA Biotech of any product performance issues observed or experienced within 30 days of receipt of said product. To see additional details on this or any of our other policies, please see our Terms & Conditions page.

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