Our Anti-Pink1 PTEN induced putative kinase 1 mouse monoclonal primary antibody from NeuroMab is produced in-house from hybridoma clone N4/15. It detects human, mouse, and rat Pink1 PTEN induced putative kinase 1, and is purified by Protein A chromatography. It is great for use in IHC, ICC, WB.
PTEN Induced Kinase 1 is encoded by the gene PINK1. PINK1 is a member of the protein kinase superfamily, Ser/Thr protein kinase family. PINK1 is a serine/threonine protein kinase that protects against mitochondrial dysfunction during cellular stress by phosphorylating mitochondrial proteins. PINK1 is highly expressed in the heart, skeletal muscle, and testis. Diseases associated with PINK1 include Parkinson Disease 6, Autosomal Recessive Early-Onset and Parkinson Disease 2, Autosomal Recessive Juvenile.
Purified by Protein A chromatography
1 mg/mL
Monoclonal
N4/15
IgG1
ICC, IHC
Mouse
PINK1
63 kDa
Fusion protein amino acids 112-496 of human Pink1 (accession number NP_115785) produced recombinantly in E. Coli
Human, Mouse, Rat
AB_10676107
Aliquot and store at ≤ -20°C for long term storage. For short term storage, store at 2-8°C. For maximum recovery of product, centrifuge the vial prior to removing the cap.
Liquid
Produced by in vitro bioreactor culture of hybridoma line followed by Protein A affinity chromatography. Purified mAbs are >90% specific antibody.
10 mM Tris, 50 mM Sodium Chloride, 0.065% Sodium Azide pH 7.4
Unconjugated
No cross-reactivity reported
Each new lot of antibody is quality control tested on cells overexpressing target protein and confirmed to give the expected staining pattern.
These antibodies are to be used as research laboratory reagents and are not for use as diagnostic or therapeutic reagents in humans.
Okatsu, K., et al. 2012. PINK1 autophosphorylation upon membrane potential dissipation is essential for Parkin recruitment to damaged mitochondria.. Nature Communications, 1016.
Malty, R.H., et al. 2017. A Map of Human Mitochondrial Protein Interactions Linked to Neurodegeneration Reveals New Mechanisms of Redox Homeostasis and NF-κB Signaling. Cell Systems, 564-577.
Henderson, M.X., et al. 2017. Unbiased Proteomics of Early Lewy Body Formation Model Implicates Active Microtubule Affinity-Regulating Kinases (MARKs) in Synucleinopathies. Journal of Neuroscience, 5870-5884.
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