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Merck

S5566

Sigma-Aldrich

Anti-α-Synuclein antibody, Mouse monoclonal

clone Syn211, purified from hybridoma cell culture

Sinónimos:

Anti-SNCA

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About This Item

Número MDL:
Código UNSPSC:
12352203
NACRES:
NA.41

origen biológico

mouse

Nivel de calidad

conjugado

unconjugated

forma del anticuerpo

purified immunoglobulin

tipo de anticuerpo

primary antibodies

clon

Syn211, monoclonal

formulario

buffered aqueous solution

mol peso

antigen 19 kDa

reactividad de especies

zebra finch, human

no debe reaccionar con

rat, mouse

envase

antibody small pack of 25 μL

concentración

~1 mg/mL

técnicas

immunohistochemistry: suitable
immunoprecipitation (IP): suitable
western blot: 0.25 μg/mL using recombinant human α·-synuclein.

isotipo

IgG1

Nº de acceso UniProt

Condiciones de envío

dry ice

temp. de almacenamiento

−20°C

modificación del objetivo postraduccional

unmodified

Información sobre el gen

human ... SNCA(6622)

Descripción general

The SNCA (synuclein α) gene codes for a 140-amino acid protein α-synuclein, that is mapped to human chromosome 4q21-23.
The SNCA (synuclein α) gene is mapped to human chromosome 4q22.1. The gene encodes a small synaptic protein called α-synuclein.

Inmunógeno

recombinant human α synuclein.

Aplicación

Anti-α-Synuclein antibody, Mouse monoclonal has been used in western blotting and ELISA.
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Flow cytometry/Cell sorting (1 paper)
Immunocytochemistry (1 paper)

Acciones bioquímicas o fisiológicas

Accumulation of α-synuclein in oligodendrocytes results in the loss of myelin and causes neurodegeneration, leading to multiple system atrophy. Synuclein-α is known to induce oligodendrocyte maturation. The encoded protein is considered to be an important aggregate of Lewy bodies, contributing to the pathogenesis of Parkinson disease.
Synuclein-α is known to induce oligodendrocyte maturation. Accumulation of α-synuclein in oligodendrocytes results in the loss of myelin and causes neurodegeneration, leading to multiple system atrophy. Mutations in the SNCA gene results in Parkinson′s disease.

Forma física

Solution in 0.01 M phosphate buffered saline pH 7.4, containing 1 % bovine serum albumin and 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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Opcional

Código de clase de almacenamiento

10 - Combustible liquids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Visite la Librería de documentos

Kavita Prasad et al.
Brain pathology (Zurich, Switzerland), 22(6), 811-825 (2012-03-29)
The role of Lewy bodies, Lewy neurites and α-synuclein (αSYN) in the pathophysiology and diagnosis of Parkinson's disease (PD) is unclear. We used postmortem human tissue, a panel of antibodies (Abs) and confocal microscopy to examine the three-dimensional neurochemical anatomy
Regional deficiencies in chaperone-mediated autophagy underlie α-synuclein aggregation and neurodegeneration
Malkus KA, et al.
Neurobiology of Disease, 46(3), 732-744 (2012)
Interactions of Pathological Hallmark Proteins
Olah J, et al.
The Journal of Biological Chemistry, 286(39), 34088-34100 (2011)
α-synuclein in blood and brain from familial Parkinson disease with SNCA locus triplication.
Miller DW, et al.
Neurology, 62(10), 1835-1838 (2004)
Sabrina Büttner et al.
The EMBO journal, 32(23), 3041-3054 (2013-10-17)
Malfunctioning of the protein α-synuclein is critically involved in the demise of dopaminergic neurons relevant to Parkinson's disease. Nonetheless, the precise mechanisms explaining this pathogenic neuronal cell death remain elusive. Endonuclease G (EndoG) is a mitochondrially localized nuclease that triggers

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