PARK7/DJ1 Antibody [D23K10] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat, Hamster, Monkey

Lane 1: MEF, Lane 2: MEF (KO DJ-1), Lane 3: Hela, Lane 4: C6

Usage Information

Dilution
WB1:1000 IP1:100 IF1:100

Application
WB, IP, IF

Reactivity
Human, Mouse, Rat, Hamster, Monkey

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
22 kDa

Datasheet & SDS

Biological Description

Specificity
PARK7/DJ1 Antibody [D23K10] detects endogenous levels of total PARK7/DJ1 protein.

Clone
D23K10

Synonym(s)
Parkinson disease protein 7; Maillard deglycase; Oncogene DJ1; Parkinsonism-associated deglycase; Protein DJ-1 (DJ-1); Protein/nucleic acid deglycase DJ-1; PARK7

Background
PARK7/DJ-1, a ubiquitously expressed dimeric protein with a conserved α-helical fold featuring a flexible nucleophile-sensing cysteine, functions primarily as an oxidative stress sentinel that maintains redox homeostasis, mitochondrial integrity, and protein quality control across neurons and peripheral tissues. Upon reactive oxygen species accumulation, DJ-1 undergoes selective oxidation at Cys106 to form a stable sulfinate that enhances dimer stability and catalytic reactivity, enabling it to directly scavenge H2O2 while allosterically activating Nrf2 transcription by disrupting Keap1 sequestration; this unleashes antioxidant response element-driven genes encoding SOD1/2, GPx, and NQO1 for cytoprotection. Concurrently, oxidized DJ-1 stabilizes the Trx1-ASK1 inhibitory complex to block MAPK/JNK-mediated apoptosis while promoting PI3K/Akt signaling through PTEN oxidation, fostering cell survival and dopaminergic neuron resilience under mitochondrial stress. DJ-1 translocates to mitochondria under paraquat or rotenone exposure to chaperone α-synuclein aggregation and facilitate mitophagy via Parkin recruitment, while nuclear accumulation coactivates androgen receptor and p53-dependent transcription for neuroprotection and DNA repair. DJ-1 sustains dopaminergic function in substantia nigra through D2 receptor trafficking and long-term depression while protecting erythrocytes from oxidant-induced hemolysis during erythropoiesis. Loss-of-function mutations cause early-onset recessive Parkinson's through failed Nrf2 induction and α-synucleinopathy, while peripheral neuropathy arises from impaired sensory neuron cold tolerance.

Background

PARK7/DJ-1, a ubiquitously expressed dimeric protein with a conserved α-helical fold featuring a flexible nucleophile-sensing cysteine, functions primarily as an oxidative stress sentinel that maintains redox homeostasis, mitochondrial integrity, and protein quality control across neurons and peripheral tissues. Upon reactive oxygen species accumulation, DJ-1 undergoes selective oxidation at Cys106 to form a stable sulfinate that enhances dimer stability and catalytic reactivity, enabling it to directly scavenge H2O2 while allosterically activating Nrf2 transcription by disrupting Keap1 sequestration; this unleashes antioxidant response element-driven genes encoding SOD1/2, GPx, and NQO1 for cytoprotection. Concurrently, oxidized DJ-1 stabilizes the Trx1-ASK1 inhibitory complex to block MAPK/JNK-mediated apoptosis while promoting PI3K/Akt signaling through PTEN oxidation, fostering cell survival and dopaminergic neuron resilience under mitochondrial stress. DJ-1 translocates to mitochondria under paraquat or rotenone exposure to chaperone α-synuclein aggregation and facilitate mitophagy via Parkin recruitment, while nuclear accumulation coactivates androgen receptor and p53-dependent transcription for neuroprotection and DNA repair. DJ-1 sustains dopaminergic function in substantia nigra through D2 receptor trafficking and long-term depression while protecting erythrocytes from oxidant-induced hemolysis during erythropoiesis. Loss-of-function mutations cause early-onset recessive Parkinson's through failed Nrf2 induction and α-synucleinopathy, while peripheral neuropathy arises from impaired sensory neuron cold tolerance.

References
https://pubmed.ncbi.nlm.nih.gov/39486088/ https://pubmed.ncbi.nlm.nih.gov/32612601/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%