AB5086
Anti-Synuclein β Antibody
serum, Chemicon®
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About This Item
Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Produtos recomendados
fonte biológica
rabbit
Nível de qualidade
forma do anticorpo
serum
tipo de produto de anticorpo
primary antibodies
clone
polyclonal
reatividade de espécies
human, rat
fabricante/nome comercial
Chemicon®
técnica(s)
immunohistochemistry: suitable
western blot: suitable
nº de adesão NCBI
nº de adesão UniProt
Condições de expedição
dry ice
modificação pós-traducional do alvo
unmodified
Informações sobre genes
human ... SNCB(6620)
Especificidade
Specific for beta-synuclein. Less than 0.1% cross reactivity against human alpha-synuclein.
Imunogênio
Synthetic peptide corresponding to the carboxyl terminal of human beta-synuclein (IEPLMEPEGSYEDPPQE).
Aplicação
Anti-Synuclein Antibody, β is an antibody against Synuclein for use in WB, IH.
Immunohistochemistry: 1:500-1:2,000
Western blot: 1:500-1:2,000
Optimal working dilutions must be determined by the end user.
Western blot: 1:500-1:2,000
Optimal working dilutions must be determined by the end user.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Neurodegenerative Diseases
forma física
Rabbit serum. Lyophilized, no preservatives. Reconstitute with 50 μL of sterile distilled water. Centrifuge to remove any residue.
Armazenamento e estabilidade
Maintain lyophilized material at -20 to -70°C for up to 12 months after date of receipt. After reconstitution maintain at -20°C in undiluted aliquots for up to 6 months. Avoid repeated freeze/thaw cycles. Glycerol (ACS grade or better) can be added (1:1) for additional stability.
Informações legais
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Exoneração de responsabilidade
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 classe de armazenamento
11 - Combustible Solids
Classe de risco de água (WGK)
WGK 1
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
Certificados de análise (COA)
Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.
Já possui este produto?
Encontre a documentação dos produtos que você adquiriu recentemente na biblioteca de documentos.
Beta-synuclein occurs in vivo in lipid-associated oligomers and forms hetero-oligomers with alpha-synuclein.
E Israeli, R Sharon
Journal of Neurochemistry null
Divya Pathak et al.
eNeuro, 4(2) (2017-05-04)
Increased α-synuclein (αsyn) and mitochondrial dysfunction play central roles in the pathogenesis of Parkinson's disease (PD), and lowering αsyn is under intensive investigation as a therapeutic strategy for PD. Increased αsyn levels disrupt mitochondria and impair respiration, while reduced αsyn
Darren C Robertson et al.
Journal of neurochemistry, 89(5), 1126-1136 (2004-05-19)
The growing body of evidence suggests that intermediate products of alpha-synuclein aggregation cause death of sensitive populations of neurones, particularly dopaminergic neurones, which is a critical event in the development of Parkinson's disease and other synucleinopathies. The role of two
Michael K Lee et al.
Proceedings of the National Academy of Sciences of the United States of America, 99(13), 8968-8973 (2002-06-27)
Mutations in alpha-synuclein (alpha-Syn) cause Parkinson's disease (PD) in a small number of pedigrees with familial PD. Moreover, alpha-Syn accumulates as a major component of Lewy bodies and Lewy neurites, intraneuronal inclusions that are neuropathological hallmarks of PD. To better
Patricia A Trimmer et al.
Journal of neurochemistry, 88(4), 800-812 (2004-02-06)
Many models of Parkinson's disease (PD) have succeeded in replicating dopaminergic neuron loss or alpha-synuclein aggregation but not the formation of classical Lewy bodies, the pathological hallmark of PD. Our cybrid model of sporadic PD was created by introducing the
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