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P0076

Sigma-Aldrich

Anti-PINK1 antibody produced in rabbit

enhanced validation

~1.5 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-BRPK, Anti-PARK6, Anti-PTEN-induced putative kinase protein 1, Anti-Serine/threonine-protein kinase PINK1, mitochondrial precursor

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~60 kDa

species reactivity

mouse (predicted), human, rat (predicted)

enhanced validation

recombinant expression
Learn more about Antibody Enhanced Validation

concentration

~1.5 mg/mL

technique(s)

western blot: 1-2 μg/mL using HEK-293T cell lysate expressign human PINK1

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... PINK1(65018)
mouse ... Pink1(68943)
rat ... Pink1(298575)

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General description

PTEN induced putative kinase 1 (PINK1) is a serine/threonine kinase expressed in mitochondria. It contains an N-terminal mitochondrial targeting motif and a highly conserved kinase domain homologous to serine/threonine kinases of the Ca2+/calmodulin family.

Application

Anti-PINK1 antibody produced in rabbit has been used in immunoblotting.

Biochem/physiol Actions

PINK1 (PTEN induced putative kinase 1, also known as PARK6 and BRPK), has been identified as linked to the autosomal recessive form of familial Parkinson disease (PD). PINK1 localized to the mitochondria protects cells from stress-induced mitochondrial dysfunction. Overexpression of wild-type PINK1 has been found to protect neurons from stress-induced mitochondrial dysfunction and apoptosis. Genetic studies in drosophila indicate that PINK1 acts upstream of Parkin in a common pathway that influences mitochondrial morphology. PINK1 activity has been shown to protect primary neurons in mouse from the dopaminergic neurotoxin MPTP (1-methyl-4-phenylpyridine (MPP+)/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) both in vitro and in vivo. This protective activity requires PINK1 kinase activity, as a PINK1 G309D mutant linked to familial PD or a kinase dead mutant K219M are not protective. PINK1 has been shown to be cleaved and localized to the mitochondria, in response to enhanced proteasomal stress in vitro and correlates with increased expression of the processed PINK1 protein in PD brain.

Target description

PINK1 is a Ser/Thr kinase that has beenlocalized to the mitochondria, and thought to protectcells from stress-induced mitochondrial dysfunction.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Mutations in PTEN-induced putative kinase 1 associated with recessive parkinsonism have differential effects on protein stability
Beilina A, et al.
Proceedings of the National Academy of Sciences of the USA, 102(16), 5703-5708 (2005)
PINK1 protein in normal human brain and Parkinson's disease
Gandhi S, et al.
Brain, 129(7), 1720-1731 (2006)
Ning Ma et al.
Frontiers in pharmacology, 12, 768700-768700 (2021-12-04)
Previously, Our study has showed that farrerol can activate Nrf2 and ameliorate cisplatin-induced acute kidney injury (AKI). Mitophagy reportedly can prevent diabetic nephropathy, cisplatin-induced AKI and other related nephropathy. In this study, we evaluated the correlation between mitophagy and the
Ying Wang et al.
Redox biology, 38, 101767-101767 (2020-11-03)
Sepsis is the major cause of acute kidney injury (AKI) associated with high mortality rates. Mitochondrial dysfunction contributes to the pathophysiology of septic AKI. Mitophagy is an important mitochondrial quality control mechanism that selectively eliminates damaged mitochondria, but its role
PINK1/Parkin-mediated mitophagy is activated in cisplatin nephrotoxicity to protect against kidney injury
Wang Y, et al.
Cell Death & Disease, 9(11), 1113-1113 (2018)

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