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Merck

P0075

Sigma-Aldrich

Anti-PINK1 (N-terminal) antibody produced in rabbit

enhanced validation

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

Sinónimos:

Anti-BRPK, Anti-PARK6, Anti-PTEN-induced putative kinase 1

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About This Item

Código UNSPSC:
12352203
NACRES:
NA.41

origen biológico

rabbit

conjugado

unconjugated

forma del anticuerpo

affinity isolated antibody

tipo de anticuerpo

primary antibodies

clon

polyclonal

Formulario

buffered aqueous solution

mol peso

antigen ~60 kDa

reactividad de especies

human

envase

antibody small pack of 25 μL

validación mejorada

recombinant expression
Learn more about Antibody Enhanced Validation

concentración

~1.5 mg/mL

técnicas

western blot: 4-8 μg/mL using HEK-293T cell lysate expressing human PINK1

Nº de acceso UniProt

Condiciones de envío

dry ice

temp. de almacenamiento

−20°C

modificación del objetivo postraduccional

unmodified

Información sobre el gen

human ... PINK1(65018)

Descripción general

PINK1 (PTEN induced putative kinase 1, also known as PARK6, BRPK), has been identified as linked to the autosomal recessive form of familial Parkinson′s disease (PD). PINK1 is a Ser/Thr kinase that has been localized to the mitochondria. PINK1 contains an N-terminal mitochondrial targeting motif and a highly conserved kinase domain homologous to Ser/Thr kinases of the Ca2+/calmodulin family.

Aplicación

Anti-PINK1 (N-terminal) antibody produced in rabbit has been used in immunoblotting.

Acciones bioquímicas o fisiológicas

PINK1 (PTEN induced putative kinase 1) has been found to protect neurons from stress-induced mitochondrial dysfunction and apoptosis. It may protect cells from stress-induced mitochondrial dysfunction. Genetic studies in Drosophila indicate that PINK1 acts upstream of Parkin in a common pathway that influences mitochondrial morphology. PINK1 elicits protection in mouse primary neurons from the dopaminergic neurotoxin 1-methyl-4-phenylpyridine (MPP+)/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) both in vitro and in vivo. In response to enhanced proteasomal stress in vitro, PINK1 has been shown to be cleaved and localized to the mitochondria, and this correlates with increased expression of the processed PINK1 protein in Parkinson′s disease (PD) brain.

Forma física

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

Cláusula de descargo de responsabilidad

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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Código de clase de almacenamiento

10 - Combustible liquids

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Equipo de protección personal

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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Visite la Librería de documentos

Altered cleavage and localization of PINK1 to aggresomes in the presence of proteasomal stress
Muqit MMK, et al.
Journal of Neurochemistry, 98(1), 156-169 (2006)
Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin
Park J, et al.
Nature, 441(7097), 1157-1157 (2006)
Cytoplasmic Pink1 activity protects neurons from dopaminergic neurotoxin MPTP
Haque ME, et al.
Proceedings of the National Academy of Sciences of the USA, 105(5), 1716-1721 (2008)
Hereditary early-onset Parkinson's disease caused by mutations in PINK1
Valente EM, et al.
Science (New York, N.Y.), 304(5674), 1158-1160 (2004)
Cristina Guardia-Laguarta et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 39(36), 7074-7085 (2019-07-14)
Maintaining a pool of functional mitochondria requires degradation of damaged ones within the cell. PINK1 is critical in this quality-control process: loss of mitochondrial membrane potential causes PINK1 to accumulate on the mitochondrial surface, triggering mitophagy. However, little is known

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